The initial clinical assessment is directed at establishing the type of chest wall deformity. This is achieved by determining the relationship of the sternum to its connecting costal cartilages. Where the sternum is posterior to the adjacent costal cartilages, the deformity is called a depression deformity (Fig. 19.1), and where it is anterior to them, it is described as a protrusion deformity (Fig. 19.2). In the latter case, one part of the sternum may be involved to a greater degree than the rest. Where it is angulated forwards in its upper part, it is termed a high protrusion. The sternum below this level may appear to produce a depression, but this is only relative as the sterno-xiphisternal junction is placed normally. In other situations, the site of maximal protrusion is at the sterno-xiphisternal junction, often with prominent adjacent costal cartilages on one or both sides and rotation of the sternum. Low sternal protrusion may be secondary to intrathoracic pathology, for example, asthma, cystic fibrosis, cystic lung, congenital cardiac disease or intrathoracic malignancy, and these conditions should be ruled out on history, examination and chest x-ray. In other types, the chest wall deformity is the primary lesion, and there is no associated intrathoracic pathology, although in Marfan syndrome, there may be a mild coexisting depression deformity.

Once the type of deformity has been established, the following features should be more exactly defined: the vertical extent of the deformity, the level of its greatest extent, the degree of asymmetry, the rotation of the sternum, the prominence of the costal cartilages, the degree of hollowing of the rib cage lateral to the sterno-xiphisternal junction, the flaring of the lower costal cartilages and the degree of postural kyphosis and scoliosis. Asymmetry occurs when the sternum is rotated in its longitudinal axis to make the costal cartilages prominent on one side and recessive on the other (Fig. 19.3). In depression deformities, the sulcus lateral to the ­sterno-xiphisternal junction is produced by the attachments of the diaphragm to the inner surface of the costal cartilages, and below this the costal margin is everted.

Most children with depression deformities are male, thin, have muscular and ligamentous laxity and poor posture. In infants with severe depression deformities, there may be paradoxical sternal retraction on inspiration.

Progression of depression deformities with growth is unpredictable, whereas primary protrusion deformities have a tendency to spontaneous improvement. Where the deformity results from an intrathoracic lesion, treatment of the cause usually results in resolution of the deformity. Absence of breast, muscle, cartilage or bone indicates a deficiency deformity, such as Poland syndrome (Fig. 19.4). In this condition, syndactyly and hypoplasia of the ipsilateral upper limb may be present as well.

An algorithm of the approach to a patient with a chest wall deformity is shown in Fig. 19.5.

Scoliosis, or lateral curvature of the spine, is common in adolescent girls where there is a genetic defect in spinal structure. Scoliosis also may be compensatory or postural in origin, which can be distinguished from structural scoliosis on clinical examination (Table 19.2).

In assessing scoliosis, the child is examined first for evidence of compensatory scoliosis. In young children, compensatory scoliosis often is caused by torticollis, following thoracotomy or when the legs are of unequal length. Torticollis is recognized on examination of the neck (see Chap. 9) and thoracotomy by a scar on the chest. To determine whether the legs are of equal length, the child stands with both feet on a firm, level surface, and the anterior or posterior iliac spines are palpated (Fig. 19.7). The bony landmarks are level if the legs are equal in length, but are at different heights when one leg is shorter than the other.