Nutritional Infant Rickets

Subarna Debbarma (BPT, DNHE)
Nutritional Infant Rickets

Rickets is a metabolic disorder of children younger than 4 years, which is caused due to the deficiency of calcium and phosphate. In rickets, the osteoid formation in the bones is normal but its mineralization is defective. This results in the formation of uncalcified bone matrix. There is an arrest of activity of the growth plate cartilage resulting in retardation of the ossification bone growth. There is softening of bone which causes deformi- ties of long bones.

Nutritional rickets is the most common type of rickets seen in developing countries. It is caused by deficiency of vitamin D. Vitamin D deficiency results from lack of dietary intake and insuf- ficiency of exposure of the body to sunlight.

The absorption of calcium and phosphate from the intestine is reduced due to deficiency of vitamin D. A fall in the level of blood calcium stimulates hypersecretion of PTH. This, in turn, mobilizes calcium from the bone, which leads to deficient calcium in the bone; making them soft and easily malleable to pressure or body weight. This causes typical deformities in the weight-bearing bones.

Clinical Features: The child is inactive/apathetic, has abnormal dentition and muscle weakness due to loss of muscle power. The bones may get fractured or deformed due to weakness of bones.

The common deformities in infantile rickets :

1. Skull

(a) Craniotabes: The fontanelle remains open even after the age of 2 years.
(b) Frontal bossing: There is prominence (bossing) of the frontal and parietal bones.

2. Chest

(a) Pigeon chest: The thoracic cage is compressed at the sides, and is raised and elongated anteroposteriorly, the sternum being prominent and thrusted forward.

(b) Rickety rosary: Bony enlargement occurs at the junction of the ribs with cartilages. It gives an appearance of a 'rosary', hence the name.

(c) Harrison sulcus: It is a transverse groove in the anterior part of the lower chest, caused by the muscular pull of the diaphragm.

3. Spine: Kyphosis involving both the thoracic and lumbar spines may be present which may subsequently lead to lumbar lordosis as the child starts walking. 

4. Abdomen: The abdomen is protuberant and gives a 'pot-belly' appearance; largely due to muscular hypotonia.

5. Upper limb: There is widening at the epiphyseal regions ofthe wrist 

6. Lower limb: Deformities like coxa vara, genu varum, genu valgum , bow-legs or forward bowing of tibia and flat feet occur due to the compressive pressure of the body weight on soft decalcified bones . Occasionally, a peculiar deformity called wind-swept deformity of genu valgum on one side and genu varum on the contralateral knee may be seen .

7. Pelvis: The size of the pelvis may be reduced; the overall growth of the child is arrested, all resulting in stunted growth or dwarfism.

Overall, the child looks weak, sick, irritable, morose and stunted in growth .

Blood serum chemistry: Serum calcium level may be normal or low but the serum phosphate is low. Serum alkaline phospha- tase is markedly raised during the active stage of the disease. 
Radiography: Radiograph of the wrist shows widening of the epiphyseal plate with fluffy and irregular edges. There is 'cupping' of the metaphysis.
Medical treatment: Administration of high doses of vitamin D with calcium supplements is the mainstay of treatment.

Orthopaedic treatment: Mild deformities in the limbs should be treated by the use of splints (Mermaid splint). Marked deformities may need surgical correction by corrective osteotomy.

Fractures are treated by adequate immobilization by plaster of Paris (POP).

Physiotherapy Management of Rickets

Prevention of deformities (at the trunk and limbs) Maintain or improve muscle functions and ROM

■Functional re-education

Early stage: The most important stage when a sick and irritable child is likely to develop multiple problems such as general debil- ity, hypotonia, weakness of the proximal limb muscles and the spinal group of muscles.

1. Therefore, correct education of the mother as regards posi- tioning, handling and carrying the child and not allowing weight bearing is important to prevent limb deformities or even fractures.

2. General body exposure to UV rays at subthermal dose of 3300-2900 A is useful.
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 infec- tion. As 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 pos- sible (e.g., kicking a 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 evi- dence of calcification.

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 frac- tures and correct deformities by osteotomy.

Appropriate physiotherapeutic measures of progressive mobili- zation and strengthening of the related muscle groups 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 train- ing, which could be gradually waned and discarded later.

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