Classification of Rickets

Degree of severity	Period of disease	Course
Mild Moderate Severe	Initial Height of disease Convalescence Residual symptoms	Acute Subacute Recurring

Clinical manifestations. Osseous changes of rickets can be recognized after several months of vitamin D deficiency. In breast-fed infants whose mothers have osteomalacia rickets may develop within 2 mo. Florid rickets appears toward the end of the 1st and during the 2-nd year of life. Later in childhood, manifest vitamin D deficient rickets is rare.

One of the early signs of rickets, craniotabes, is due to thinning of the outer table of the skull and detected by pressing firmly over the occiput or posterior parietal bones. A ping-pong-ball sensation will be felt. Craniotabes near the suture lines is a normal variant. Low-birthweight infants are particularly susceptible to the early development of rickets and to craniotabes. Palpable enlargement of the costochondral junctions (the "rachitic rosary") and thickening of the wrists and ankles are other early evidences of osseous changes. Increased sweating, particularly around the head, may also be present.

Head. Craniotabes may disappear before the end of the 1st year, although the rachitic process continues. The softness of the skull may result in flattening and, at times, permanent asymmetry of the head. The anterior fontanel is larger than normal; its closure may be delayed until after the 2nd year of life. The central pans of the parietal and frontal bones are often thickened, forming prominences or bosses, which give the head a boxlike appearance (caput quadratum). The head may be larger than normal and may remain so throughout life. Eruption of the temporary teeth may be delayed, and there may be defects of the enamel and extensive caries. The permanent teeth that are calcifying may also be affected; the permanent incisors, canines, and first molars usually show enamel defects.

Thorax. Enlargement of the costochondral junctions may become prominent; the beading of the ribs is not only palpable but also visible. The sides of the thorax become flattened, and the longitudinal grooves develop posterior to the rosary. The sternum with its adjacent cartilage appears to be projected forward producing the so-called pigeon breast deformity. Along the lower border of the chest develops a horizontal depression, Harrison's groove which corresponds with the costal insertions of the diaphragm. There may be a variety of other thoracic deformities, including those of the shoulder girdle.

Spinal Column. Slight to moderate degrees of lateral curvature (scoliosis) are common, and a kyphosis may appear in the dorsolumbar region of rachitic children when sitting. Lordosis of the lumbar region may be seen in the erect position.

Pelvis. In children with lordosis there is frequently a concomitant deformity of the pelvis, which is also retarded in growth. The pelvic entrance is narrowed by a forward projection of the promontory the exit, by a forward displacement of the caudal part of the sacrum and the coccyx. In the female, these changes, if they become permanent, add to the hazards of childbirth and may necessitate cesarean section.

Extremities. As the rachitic process continues, the epiphyseal enlargement at the wrists and ankles becomes more noticeable. The enlarged epiphyses can be seen or palpated but are not distinct in roentgenograms because they consist of cartilage and uncalcified osteoid tissue. Bending of the softened shafts of the femur, tibia, and fibula results in bow-legs or knock-knees; the femur and the tibia may also acquire an anterior convexity. Coxa vara is sometimes the result of rickets. Greenstick fractures occur in the long bones; often there are no clinical symptoms.

Deformities of the spine, pelvis, and legs result in reduced stature, rachitic dwarfism.

Ligaments. Relaxation of ligaments helps to produce deformities and partly accounts for knock-knees, overextension of the knee joints, weak ankles, kyphosis, and scoliosis.

Muscles. The muscles are poorly developed and lack tone. As a result, children with moderately severe rickets are late in standing and walking. Potbelly depends to a large extent on weakness of the abdominal muscles; weakness of the gastric and intestinal walls may contribute.