This document discusses rickets, a disease caused by vitamin D deficiency or impaired mineralization that affects growing bones in children. It defines rickets and outlines various types including nutritional, vitamin D dependent, and vitamin D resistant rickets. Clinical features like softening of bones and skeletal deformities are described. Laboratory findings of low calcium and phosphorus and high alkaline phosphatase are also summarized. The document outlines prevention through diet, supplementation, and sunlight exposure as well as treatment with high dose vitamin D or calcium therapy.

1. RRIICCKKEETTSS

2. LLEEAARRNNIINNGG OOBBJJEECCTTIIVVEESS
• Define Rickets
• Enumerate types of Rickets
• Describe clinical features of nutritional
Rickets
• Explain lab diagnosis and X-ray findings in
nutritional rickets
• Describe preventive measures for
nutritional rickets
• Enlist the post Rickets deformities in
musculoskeletal system.

3. DDEEFFIINNIITTIIOONN
Rickets
A disease of growing bones
occurs in children
before fusion of epiphysis
due to
un mineralized matrix
at the growth plates.
.

4. OOsstteeoommaallaacciiaa
Failure of mature bones to mineralize
due to
prolonged deficiency
dietary lack of vitamin D
or
lack of ultraviolet rays of sun.

5. VVIITTAAMMIINN DD MMEETTAABBOOLLIISSMM
Maintenance of normal plasma levels of
Calcium & phosphorus.
Two forms of Vit D are present
1 Vit D2 (ergocalciferol)
2.Vit D3 (cholecalciferol)

7. • In liver it is hydroxylated into 25-
hydroxycholicalciferol(25 OH-D)
• Converted in the kidney into 1-25-(OH)2-D
• The most active metabolite of Vit D
• It acts on GIT to increase calcium
absorption
• On bone to increase calcium resorption
• Parathyroid hormone activates Alpha-1
hydroxylase enzyme in the kidney.

8. TTyyppeess ooff RRiicckkeettss
• Vitamin D Deficient Rickets(nutritional)
• Vitamin D Dependent rickets
• Vitamin D Resistant Rickets
• Renal Rickets
• Hepatic Rickets
• Congenital Rickets

9. NNoorrmmaall bboonnee ddeevveellooppmmeenntt
• Bone consists of protein matrix –osteoid
• Mineral phase-calcium and phosphorus.
• Ossification
• Intramembranous ossification-flat bones
mesenchymal cells differentiate into
osteoblasts
• Enchondral ossification –long tubular
bones

10. EEnnddoocchhoonnddrraall oossssiiffiiccaattiioonn
• Growing cartilage at the epiphyseal plates
is mineralized and resorbed
and
replaced by osteoid matrix
which undergoes mineralization
to create bone.

11. IInn RRiicckkeettss
Mineralization is delayed or inadequate
osteoid thickens and increase in
circumference of growth plate.
Softening of the bones-----Deformities

12. CCLLIINNIICCAALL FFEEAATTUURREESS
• Peak incidence 6 months – 2 years
• Irritability
• profuse sweating while asleep
• hypotonia
• frequent respiratory infections.
• Failure to thrive
• Delay in walking,delayed dentition
• Fits,tetany.

13. SSIIGGNNSS
HEAD
• Larger than normal.
• Frontal bossing (due to excess osteoid)
Craniotabes (ping pong ball sensation)
due to thinning of outer table of skull.
• Delayed closure of anterior fontanel
• caput quadratum (square like head)

15. TTHHOORREEXX
• Rachitic Rosery (prominent costochondral
junctions)
• Harrison’s sulcus (depression above the
subcostal margin at the site of diaphragm)
Pulling of softened ribs by the diaphragm during
inspiration.
• Pigeon chest deformity.(The weakened ribs
bend inwards due to the pull of respiratory
musclesand ,causing anterior protrusion of
sternum.

19. EExxttrreemmiittiieess
1. Widening of wrists and ankles
2. Bending of long bones
results in
bow legs
knock knees,(genu valgum)
3. Green stick fractures

20. WWiiddeenniinngg ooff wwrriisstt jjooiinnttss

21. WWiiddeenniinngg ooff aannkkllee jjooiinnttss

28. LLAABB DDAATTAA
1.Serum Calcium low (normal 9-11mg/dl)
2.Serum phosphorus low (normal-5-7mg/dl
3.Alkaline phosphatase is raised.
This is the most striking feature,shows
increased but ineffective activity of
osteoblasts.
4. 25-(OH) D levels less than 20 ng/dl
Confirms of Vitamin D deficiency

30. TTYYPPEE 22 VVIITT DD DDEEPPEENNDDEENNTT
• End Organ resistance to effects to 1,25.
(OH) –D3
• ALOPECIA
• 1-25(OH) VIT D is high
• TREATMENT
• Physiological doses of one alpha Leo
• 1-2 micrograms per day.

31. PPRREEVVEENNTTIIOONN
• To prevent rickets, health experts
recommend
• a child should be breast-fed
• weaned and put on to cow's milk and
other foods rich in vitamin D and calcium,
like eggs and dairy products such as
butter and leafy vegetables.
• Fish

32. PPRREEVVEENNTTIIOONN
• Daily intake of 400 i.u.vitamin D by
supplemention.
• Lactating mothers should receive
supplemention with milk or vitamin D to
ensure prevention of rickets in their
babies.
• Sun exposure to mothers.

33. • Calcium supplements such as lime can
also be added to staple foods like rice and
bread. Plenty of sunlight, fresh air and
exercise are also necessary to ensure
sufficient Vitamin D intake.

34. • A meeting of international experts on
rickets held in Dhaka in 2006 identified
community-based awareness as one of
the most effective measures against the
spread of rickets. Experts at the meeting
said efforts to boost rice production over
the years had influenced diets: there was
less emphasis on calcium-rich foods such
as dairy products and leafy green
vegetables.

36. LLEEAARRNNIINNGG OOBBJJEECCTTIIVVEESS
• Describe clinical features of rickets
• Enumerate investigations of rickets
• Interpret investigation of rickets
• Describe management of rickets.
• Identify radiological findings in rickets,
osteomalacia and osteoporosis

37. TTRREEAATTMMEENNTT
• STOSS THERAPY
• 300,000-600,000 units i/m
• Indrop D 200,000 units
• Repeat x-ray after 3 weeks
• Another dose
• HIGH DOSE VITAMIN D THERAPY
• 2000-5000 IU/day over 4-6 weeks
• Followed by intake o 400 I/U daily

38. VVIITTAAMMIINN DD DDEEPPEENNDDEENNTT
RRIICCKKEETTSS
• Inborn error of vitamin D metabolism
• Autosomal Recessive
• Type 1 and 2
• TYPE 1
• Defect in 1 alpha-hydroxylase responsible for
the synthesis of 1-25-dihydroxy vit D
• Symptoms in the 1st year of life
• Tetany,convulsions,musle weakness andgrowth
failure

39. VITAMIN DD RREESSIISSTTAANNTT RRIICCKKEETTSS
• X linked dominant
• Males are more severely effected than
females
• Vitamin D activation & tubular
reabsorption of phosphate are impaired
resulting in hypophosphatemia .
• TREATMENT
• Oral Phosphate and 1 ,25-(OH)2 –D3
0.05micrograms /kg/day.

40. PPRREEVVEENNTTIIOONN
1.Exposure to sunlight (ultraviolet light)
Early morning and evening 30 minutes per
week or 2 hours per week maintains
adequate sun exposure.
2.Food fortified with Vit A and Vit D
specially butter,ghee and milk.
Children under 5 should 500ml of milk
daily or youghart or cheese daily.