.

Rickets

� Rickets is a bone disorder caused by a deficiency of vitamin d,

calcium, or phosphate.
� In rickets the osteoid formation of the bone is normal but
mineralization is defective, caused formation of uncalcified bone
matrix.

RICKETS DR. HEMENDRA KUMAR SHARMA

ASST. PROF.
� Arrest of the activity of the growth plate resulting in retardation of
the ossifications of the long bones.
� Softening of bones causing deformity of long bones.
DEP. OF PHYSIOTHERAPY

Four main causes:

1. Vitamin D deficiency:
• Reduced dietary intake
• Reduced amount of sunlight � Vitamin D deficiency results from lack of dietary intake and
• Pigmented skin insufficiency of exposure of body to sunlight.
� Absorption of calcium and phosphate reduces due to deficiency of
2. Malabsorption due to: vitamin D.
• Celiac disease � Fall in the level of calcium stimulate high level of PTH which mobilize
calcium from bone, leads to deficient calcium in the bone
• Hepatic osteodystrophy
� Bones become soft and malleable to pressure or body weight .
3. Renal disease:
� Causes deformity in the weight bearing bones.
• Glomerular failure
• Renal osteodystrophy
4. Antiepileptic drugs favor formation of hepatic enzyme
which prevents conversion of calciferol.

� Skull :

1. Craniotabes- fontanelle remains open even after age of 2 years

Type 1 Type 2 2. Frontal bossing of frontal and parietal bones

A. Due to deficiency of vitamin D � Chest :

A. Defective absorption of Pigeon chest with prominent sternum
� Diminished intake e.g., malnutrition phosphates through renal tubules
� Diminished absorption e.g., � Hypophosphataemic rickets (x Rickety rosary – bony enlargement at the junction of ribs with cartilage.
- mal-absorption syndrome linked dominant) � Spine :

- gastric abnormalities � Fanconi syndrome Kyphosis involving both thoracic and lumbar spine may subsequently leads
� Renal tubular acidosis to lumbar lordosis
- biliary diseases
B. Due to disturbance in vitamin D � Oncogenic rickets � Pot belly appearance at the abdomen
metabolism B. Diminished intake or absorption � Upper limb: widening at the epiphyseal region of the wrist
� Hepatic factor phosphates
� Lower limb:
� Renal factor Deformities like knock knees or bow legs
� Renal osteodystrophy � Pelvis: reduced size with stunted growth or dwarfism

1

� Blood serum chemistry:
o serum calcium level may be normal or low
o serum phosphate is low
o serum alkaline phosphate is raised during
active stage of disease
� Radiological features:
X-ray of knee and wrist (AP view)
o Delayed appearance of epiphyses
o Widening of epiphyseal plates
o Cupping of metaphysis
o Splaying of metaphysis
o Rarefaction of diaphyseal cortex occurs late
o Bone deformities : knock knees, bow legs,
coxa vera in older children.
Goals :
� Prevention of deformity ( at the trunk and limbs).
� Maintain or improve muscle functions and ROM.
� Functional re-education.
3. Put the child on the floor in different positions and let it perform free
movements of the limbs and the trunk.
4. Chest physiotherapy helps in improving general health by increasing
oxygen uptake and also in preventing chest infection. All the general
condition improves, child will become more active. For chest
physiotherapy, if active exercises are not possible, passive
(gentle) breathing exercises can be given.
5. Initiate intelligent objective modes of getting purposeful functional
exercises done, offering resistance wherever possible (e.g., kicking ball).
6. Initiate controlled resistive proprioceptive neuromuscular facilitation
(PNF) patterns with guided assistance.
7. If a child attempts to stand and walk, provide orthosis or a brace to
prevent limb deformities when there is definite evidence calcification.
.
� Medical treatment:
Administration of high dose of vitamin D with calcium supplements is the mainstay
of treatment
� Orthopedic treatment :
1. Mild deformities should be treated by the use of splints (Mermaid splint)
2. Marked deformity need surgical correction by corrective osteotomy
EARLY STAGE
The most important stage when a sick and irritable child is likely to
develop multiple problems such as general debility, hypotonia,
weakness of the proximal limb muscles and the spinal group of
muscles.
1. Correct education of the mother as regards positioning, handling
and carrying the child and not allowing weight bearing important
to prevent limb deformities or even fractures.
2. General body exposure to UV rays at subthermal dose of 3300–
2900 A is useful.
LATE STAGE
Increase the vigorousity of exercise concentrating mainly on the functional muscle
groups. Continue progression till the child is functionally self-sufficient and free
from deformity.
Following surgery:
Surgery is mostly undertaken to treat fractures and correct deformities by
osteotomy.
Appropriate physiotherapeutic measures of progressive mobilization and
strengthening of the related muscle group facilitates early return of function.
Though these measures appear easy, tremendous long-standing effort is needed to
successfully manage a child with rickets. The child may be given supportive
orthoses to give ambulatory training, which could be gradually waned and discarded
later.
2
.