In this essay we will discuss about the Rickets:- 1. Meaning of Rickets 2. Risk Factors of Rickets 3. Secondary Osteomalacia and Rickets 4. Clinical Features 5. Diagnosis.
Contents:
- Essay on the Meaning of Rickets
- Essay on the Risk Factors of Rickets
- Essay on the Secondary Osteomalacia and Rickets
- Essay on the Clinical Features of Rickets
- Essay on the Diagnosis of Rickets
Essay # 1. Meaning of Rickets:
Rickets is a disease of children in which the bones are softened and deformed. It arises as a result of deficiency of Vitamin D and a failure to absorb calcium from the small intestine. Osteomalacia, which means softening of bone, arises when there is Vitamin D deficiency in adults. The resultant calcium deficiency leads to demineralization of the bones.
The severe forms of both diseases with gross deformities of the skeleton are now rare but cases may be seen occasionally in hospitals in most countries. Only a few foods are good sources of Vitamin D and about 90 per cent of the vitamin in our bodies comes from photosynthesis in the skin.
Essay # 2. Risk Factors of Rickets:
a. In northern latitudes during long winters with only a few hours of daylight greatly reduce exposure to ultraviolet radiation. Vitamin D deficiency is then a risk for all children and adolescents, as they have greater need for the vitamin than adults, and also for all elderly people and others with disabilities restricting outdoor activities.
b. Puppies developed rickets when white bread in their diet was replaced by unrefined oatmeal. Asian communities whose stable food is chapati made from high extraction wheat flour appear to be at increased risk of both rickets and osteomalacia.
c. Strict Hindus and others who eat no animal food provide an increased proportion of cases of osteomalacia seen in Britain. This complete exclusion of Vitamin D from the diet does not normally lead to rickets or osteomalacia but increases the risk.
d. When an infant is fed exclusively on milk from a Vitamin D deficient mother for more than three months, the risk of infantile rickets rises.
e. Heavy pigmentation reduces synthesis of Vitamin D in the skin. This can only be a minor risk factor since in Britain rickets is much less common in the darker West Indian than in the lighter Asian communities.
Essay # 3. Secondary Osteomalacia and Rickets:
a. Osteomalacia may arise in patients with the malabsorption syndrome after many months. This is due to impaired calcium absorption.
b. Osteomalacia and other bone disorders arise in patients with chronic renal failure. Impaired formation of 1, 25 (OH)2 D in the kidney may be responsible.
c. Osteomalacia is sometimes found in patients with cirrhosis of the liver due to failure to form 25 (OH) D.
d. Five different genetic defects that lead to rickets are known. All are uncommon.
Essay # 4. Clinical Features of Rickets:
a. The child is restless, fretful and pale, with flabby and toneless muscles which allow the limbs to assume unnatural postures (acrobatic rickets).
b. Excessive sweating on the head is common.
c. The abdomen is distended as a result of the weak abdominal muscles, the atony of the intestinal musculature and the intestinal fermentation that may arise from excessive carbohydrate in the diet.
d. Gastrointestinal upsets with diarrhoea are common.
e. The infant or child is prone to respiratory infections.
f. Development is delayed, the teeth often erupt late and there is failure to sit up, stand, crawl and walk at the normal ages.
g. There is extension and widening of the epiphyses at the growing points, where cartilage meets bone. The earliest bony lesions are usually enlargement of the epiphyses at the lower end of the radius and at the costochondral junctions of the ribs or ‘rickety rosary’, an early and important diagnostic feature. Later features are ‘bossing’ of the frontal and parietal bones and delayed closure of the anterior fontanelle.
h. There may be deformities of the chest such as undue prominence of the sternum (pigeon chest) and a transverse depression, passing from the costal cartilages towards the axillae which deepens with inspiration. In unusually severe cases, respiratory functions can be seriously impaired by the combination of respiratory infection and a rachitic chest.
i. If rickets continues into the second and third year of life, these signs may persist or be magnified. Deformities such as kyphosis of the spine develop as a result of the new gravitational and muscular strains, caused by sitting up and crawling.
At the same time there may be enlargement of the lower ends of the femur, tibia and fibula. When the rachitic child begins to walk, deformities of the shafts of the leg bones develop, so that ‘knock knees’ or ‘bow legs’ are added to the clinical picture. Anterolateral bowing of the tibiae at the junction of the middle and lower third is frequently noted in young children with rickets.
j. The spinal kyphosis is often replaced by lordosis. Pelvic deformities may follow and lead years later to serious difficulties at child birth.
k. When ionized calcium in the plasma is reduced, infantile tetany may result, with spasm of the hands and feet and of the vocal cords. The latter causes a high-pitched, distressing cry and great difficulty in breathing.
Essay # 5. Diagnosis of Rickets:
A flabby baby towards the end of its first year, unable to pull itself up, fretful and easily irritated, with too few teeth showing and liable to profuse sweats, should always be suspected of having rickets.
Early evidence of rickets may be overlooked in a child ill with bronchopneumonia or diarrhoea, especially in the first year of life. If there is any doubt, a radiograph of the wrist may show characteristic changes at the epiphyses; the outline of the joint is blurred and hazy, and the epiphyseal line becomes broadened.
Later, in older children, as a result of decalcification of the metaphysis and the effects of movements and stresses the classical metaphysis and the effects of movements and stresses the classical concave ‘saucer’ deformity is clearly shown radio-graphically.
The opinion of an experienced radiologist may be needed to distinguish the picture from that of scurvy. The diagnosis is supported by a raised plasma alkaline phosphatase and confirmed if plasma 25 (OH) D is low.
It is sometimes necessary to distinguish rickets from other rare disorders involving the bones, such as congential syphilis, achondroplasia and osteogenesis imperfecta. Radiographs of the bone are helpful in differentiating these disorders.