Rickets is the softening and weakening of bones in children, usually because of an extreme and prolonged vitamin D deficiency. Rare inherited problems also can cause rickets.
Vitamin D helps your child's body absorb calcium and phosphorus from food. Not enough vitamin D makes it difficult to maintain proper calcium and phosphorus levels in bones, which can cause rickets.
Adding vitamin D or calcium to the diet generally corrects the bone problems associated with rickets. When rickets is due to another underlying medical problem, your child may need additional medications or other treatment. Some skeletal deformities caused by rickets may require corrective surgery.
Rare inherited disorders related to low levels of phosphorus, the other mineral component in bone, may require other medications.
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Book: Mayo Clinic Family Health Book, 5th Edition
Symptoms
Signs and symptoms of rickets can include:
Delayed growth
Delayed motor skills
Pain in the spine, pelvis and legs
Muscle weakness
Because rickets softens the areas of growing tissue at the ends of a child's bones (growth plates), it can cause skeletal deformities such as:
Bowed legs or knock knees
Thickened wrists and ankles
Breastbone projection
Creeping Stroke - Venous thrombosis presenting with pc-stroke.pptx
Imaging in Rickets & Scurvy.pptx
1. Imaging in Rickets & Scurvy
Presented by- Moderator-
Dr. Shivani Gupta Dr. Shalini
Agarwal
Junior Resident 1
Dept. of Radio-diagnosis
PGIMS Rohtak
2. PHYSIS/ GROWTH PLATE
It is the anatomical
difference between growing
and mature bone.
It appears radiologically as a
lucency between the
epiphysis and the
metaphysis.
It represents the site where
longitudinal bone growth
occurs.
It is the primary site for the
effect of metabolic and
endocrine bone disorder.
3. 3 zones of
physis-
Resting/ germinal zone
Proliferating zone
Hypertrophic
zone: zone of
maturation,
degeneration and
provisional
calcification
5. INTRODUCTION
It is a disease of childhood
characterized by failure of
mineralization of osteoid tissue in
developing skeleton, particularly at the
growth plate.
Age: 6-12 months.
At risk- Dark pigmented individuals,
infants breast-fed for prolonged
periods of time by a multiparous
mother, at higher altitudes
7. PATHOLOGY
Decrease in quantity of calcified
osteoid & increase in uncalcified
osteoid.
Osteopenia
Cartilage cells at physis grow normally
but FAIL TO CALCIFY.
Growth plate is widened due to
overgrown & hypertrophied cartilage
9. CLINICAL FEATURES
First 6 months :Tetanic convulsions
Irritability, weakness
Delayed development
Small stature
Bony deformities and pain
Rachitic rosary
Swelling of wrist and costocartilage
Thoracic kyphosis with pigeon chest
Harrison’s sulcus
Greenstick fractures are common
10.
11. RADIOLOGICAL FEATURES
MC and non specific finding : osteopenia
Loss of provisional zone of calcification
Changes are seen at open growth plate
Especially visible at fast growing growth
plates like costochondral junction of the
middle ribs, knees, wrists & ankles.
Earliest sign : distal ends of radius and
ulna. Ulnar growth plate grows more
rapidly so manifestations are seen
earlier in ulnar growth plate
12. WIDENING OF GROWTH PLATE
Earliest and specific radiological
change
Due to increase in cartilaginous cell
mass and loss of normal zone of
provisional calcification
14. METAPHYSEAL CUPPINGAND
WIDENING
Protrusion of bulky
mass of
cartilageneous cells in
the zone of
hypertrophy into the
poorly mineralized
metaphysis
Cupping is common
in both ends of fibula
and distal end of ulna
and tibia
Not seen in bones of
elbow
Paint-brush
metaphysis
18. CRANIOTABES
Excess osteoid
deposition in
frontal and parietal
regions with
posterior flattening
of skull due to
supine posture of
infant
Squared
configuration of
skull
Demineralisation
of skull
19. BOWING OF LONG BONES
Cause-
Displacement of
growth centres
owing to
asymmetrical
musculotendino
us pull on the
weakened
growth plate
21. PA radiograph of both hands shows
diffuse osteopenia, cupping, fraying &
splaying of metaphyses of b/l distal
radius and ulna.
22.
23. AP Radiograph of
both lower limbs
obtained 2 years
after active disease
phase shows
bowing of tibia and
fibula and
transverse sclerotic
bands at the
metaphysis parallel
to the growth plate
(Harris growth
arrest lines or park
lines)
24. SIGNS OF HEALING RICKETS
Seen within 2-3 weeks of adequate therapy
Total calcification is usually complete in 2
months
Signs :
Reappearance of dense zone of provisional
calcification : first evidence
Increase in cupping of healing metaphysis
Recalcification of subperiosteal osteoid
resulting in thick cortex surrounding the shaft
Sharply defined ossification centres
25. FIRST E/O HEALING RICKETS:
REAPPEARANCE OF DENSE
ZONE OF PROVISIONAL
CALCIFICATION
Seen as a
transverse line of
increased density
which appears
beyond the visible
end of shaft with
metaphysis
interposed
between two
radiolucent areas
26. Complete healing and restoration of
normal structure is the rule in rickets
even if severe changes are present
during the active stage !
28. Introduction
Scurvy is a nutritional bone disorder
which occurs due to long term
deficiency of Vitamin C.
Infantile Scurvy: due to pasteurised or
boiled milk preparations
Age: 8-14 months
Latent period- 4 months before
symptoms and skeletal changes
become apparent.
29. PATHOLOGY
Vitamin C is necessary for hydroxylation of
proline to hydroxyproline which is vital for
collagen synthesis.
Vitamin C is also necessary for endothelial lining
Deficiency causes increased vascular fragility
Osteoblasts require vit C to form mature osteoid
tissue.
Decreased osteoblastic activity
Generalised osteopenia and osteoporosis
Cartilage proliferation is decreased but
mineralisation is normal.
30. Clinical features
Clinical hallmark : Spontaneous
haemorrhage i.e. cutaneous
petechiae,bleeding gums,melena &
hematuria.
Progressive irritability with tender
edematous limbs and a tendency to lie
supine & motionless with the thighs
abducted (frog-leg position,
pseudoparalysis)
Bulging at costochondral junction
(Scorbutic rosary-Sharp pain & tender)
31. WHITE LINE OF FRENKEL
Dense zone of
provisional calcification.
Radiodense line in the
zone of provisional
calcification at the
growing metaphysis
Cause- Cartilage
proliferation decreased
with normal
mineralisation.
Conversion into bone is
delayed.
32. TRUMMERFELD ZONE
(Scorbutic zone)
Transverse radiolucent
band directly beneath
the zone of provisonal
calcification.
Cause- Suppressed
osteoblastic activity
with normal
mineralisation leading
to disordered osteoid
formation.
Trabecular bone mass is
decreased.
33. PELKAN’S SPUR
Bony protuberances at
the metaphyseal
margins at right angles
to the shaft.
Cause- Zone of
provisional calcification
extends beyond the
margins of the
metaphysis resulting in
periosteal elevation
and marginal spur
formation
34. WIMBERGER'S
SIGN
(Ring epiphysis)
Epiphysis is small &
sharply marginated by
sclerotic rim with central
portion more radiolucent.
Cause- Decreased
cartilage proliferation
and unimpaired
mineralization
(sclerosis)
Differentiates healing
rickets and scurvy
35. CORNER (ANGLE) SIGN
Irregularity of the
metaphyseal
margins.
Cause- Infarctions
of the epiphyseal-
metaphyseal
junction
36. SUBPERIOSTEAL
HEMORRAGES
Seen in ends of long
bones(femur,tibia,
humerus)
May cause
periosteal elevation
and new bone
formation
Cause-Increased
capillary fragility
37.
38.
39.
40. Coronal T2-weighted fat-suppressed MR
image of both distal femoral
metadiaphyses shows heterogeneously
increased T2 signal intensity in the
marrow (*) and around the bone (arrows)
41. HEALING SCURVY
On vitamin C therapy, all changes are
reversible though a single growth
arrest line may remain in metaphysis
as residual frenkel’s line.
Following therapy, subperiosteal
hematomas rapidly calcify and
demarcate.