The Ortolani test is used to diagnose congenital dysplasia with dislocation of the hips (Fig. 13.1). The baby should be relaxed with the pelvis held still between the thumb and fingers of one hand while the other hand holds the thigh with the thumb in the groin (anteriorly) and the middle finger on the greater trochanter (posteriorly). The hip is flexed to 90° and then abducted to 45°. In this position, forward pressure with the middle finger will tend to push the femoral head into the joint, while backward pressure of the thumb will tend to dislocate the head posteriorly. When the femoral head relocates, there is an audible and palpable ‘clunk’. The baby should be referred for ultrasonography to confirm the abnormality and then for an orthopaedic opinion and application of a harness (e.g. Pavlik) to hold the femoral head within the joint until dislocation can no longer occur.

Most abnormalities are caused by extrinsic compression of the feet within the uterus and resolve spontaneously after birth (Fig. 13.2). These postural deformities can be recognized on examination by a normal range of passive movement. The deformity may be caused by abnormalities of fetal position or of the uterus (e.g. septum or fibroids) and will be predisposed to by oligohydramnios, a small amniotic cavity (especially with chromosomal abnormalities), or paralysis/stiffness of the legs (e.g. spina bifida, arthrogryposis). Weak legs cannot kick hard enough to allow the feet to maintain their normal posture in utero. Consequently, all babies with deformed feet must be examined carefully for (1) major chromosomal defects, (2) multiple joint abnormalities (arthrogryposis) and (3) myelomeningocele.

Particular postural deformities, such as calcaneovalgus, are of themselves trivial but may signal associated dislocation of the hip since the position of the dislocated leg in utero predisposes to this deformity.

Metatarsus adductus (or metatarsus varus) is a relatively minor angulation deformity of the foot caused by compression of the foot around the contralateral leg. If the foot has full passive movement, casts or splints should not be needed.

Talipes equinovarus, or ‘club foot’ (Fig. 13.3), needs to be assessed carefully since any limitation of passive movement indicates that immediate treatment is required. This is because the lax joints in the first week of life allow rapid correction with serial plaster casts or splints. If the foot cannot be pushed into the calcaneovalgus position easily, an orthopaedic surgeon should be consulted.

A common concern both of parents and of medical attendants at birth is whether the fingers and toes are normal. The likely problems are (1) incomplete separation of the fingers or toes (syndactyly), (2) duplication of the digital rays to produce an extra digit (polydactyly), (3) curly toes and (4) trigger thumb (described later).

Where syndactyly is present, the examination should include all limbs as well as enquiry about other family members because of the likelihood of familial inheritance. In addition, syndactyly is a common feature of recognized syndromes, and therefore other abnormalities should be sought during the general examination (see Chap. 2).

With polydactyly, the examination should determine whether the extra digits have a bony connection with the rest of the hand or foot. Where the base is narrow and contains no bone, ligation of the base at birth is satisfactory. Extra digits containing bone, or with a wide base, need referral for excision at a convenient time after the neonatal period.

This may be caused by (1) metatarsus adductus (medial angulation of the forefoot), (2) internal tibial torsion (spiral twist of the tibia) or (3) internal femoral torsion (spiral twist of the femur) (Fig. 13.4). Metatarsus adductus usually reflects deformity in utero and is recognized easily by inspection of the shape of the foot. It may first be noticed at the time of walking. The tibia of an infant normally grows with a slight outward curvature and a degree of internal twist or torsion. Internal tibial torsion may be exacerbated by the baby sleeping face down with the feet tucked inwards underneath or by the infant sitting on the in-turned feet. Elimination of these postures should allow the tibia to straighten normally with growth. Internal femoral torsion (‘in-set hips’) is in part an inherited condition common in girls, made worse by sitting with the legs rotated outwards for long periods of play or kindergarten activities. It resolves spontaneously with ­maturation of the pelvis and femur.

The history should include questions about (1) a family history of leg deformity, (2) any functional impairment of normal activities (there should be no impairment unless there is an underlying cause, e.g. occult spina bifida, muscular dystrophy) and (3) the common sleeping and sitting positions (are these making it worse?).

Clinical examination of a child with in-turned toes is structured to answer four questions: (1) “How severe is it?” The gait angle should be assessed by observing the feet during walking and is best done by watching from directly in front (Fig. 13.5). The normal angle between the feet during walking is 10° of external rotation. (2) “Is it the tibia or the foot?” The infant is placed prone on the couch with the knees bent. The feet are observed from above. Metatarsus adductus is revealed by the shape of the sole (Fig. 13.5). Internal tibial torsion is determined by the angle between the thigh and the foot, which is normally 0–30° of external rotation. (3) “Is it the femur?” With the knees still bent, the clinician crouches down and examines the degree of hip rotation, using the lower leg as the marker (Fig. 13.6). The normal range is 45° of internal rotation (the tibia appears externally rotated because the child is prone rather than supine) to 30° external rotation (looks like internal rotation). Where internal femoral torsion is present, the legs may lie easily on the couch (i.e. 90° internal rotation) and external rotation will be limited. (4) “Are there other abnormalities?” Hip abduction should be tested to exclude an unrecognized dislocation of the hip as the cause of in-toeing. Weak muscles causing or exacerbating the deformity should be excluded by instructing the child to sit on the floor and then to stand up (Fig. 13.7). Use of the hands in levering himself up (positive Gowers’ sign) indicates general or specific muscle weakness (e.g. muscular dystrophy). Finally, the lumbosacral spine should be examined for external stigmata of occult spina bifida (see Chap. 18).

Bowing of the tibia is extremely common before 2 years of age and resolves spontaneously in most children as the growth of the bones responds to weight-bearing. Usually, it is associated with internal torsion of the tibia (Fig. 13.4b). Rickets (vitamin D deficiency) may cause bow legs because of bone softening, but this is now rare where milk is supplemented with vitamin D. Enlargement of the growth plates at the wrists or the costochondral junctions (‘rachitic rosary’) would confirm this rare cause.

The degree of severity of bowing of the tibia can be assessed by placing the infant supine after removal of all clothes from the waist down. The legs are held with the knees extended, the knee caps pointing towards the ceiling and the medial malleoli touching each other. The distance between the knees is determined with a tape measure.

This is nearly always a normal variant during growth of the femoral condyles between 2 and 7 years, and only rarely is knock knee caused by rickets. The deformity produces no symptoms, and clumsiness is more likely to be related to neuromuscular development. The deformity reaches a peak at three and a half years, after which relative growth of the lateral condyle increases and the level of the knee joint becomes horizontal causing the legs to straighten.

The severity of the deformity is measured with the child standing and the knees touching (Fig. 13.8). The normal distance between the medial malleoli may be up to 10 cm. The feet appear to be flat because the knock knees shift the weight-bearing onto the medial side of each foot.

In fat toddlers, the feet often appear flat because of a thick fat pad on the sole.

The deformity is common early in childhood when the ligaments are loose. Once walking (and weight-bearing) is established, the strength of the arch ligaments increases, making the foot appear normal by 5–7 years.

Many ‘flat’ feet become normal when weight-bearing is maximal, such as when standing on tiptoes. These children have flexible joints with loose ligaments, but muscle strength and bony structures are normal. Pathological causes include muscle weakness or imbalance (cerebral palsy, muscular dystrophy) or rare intrinsic bony abnormalities (e.g. ‘rocker-bottom’ feet where the talus is abnormally vertical). The latter deformity may be associated with major chromosomal defects.

The feet are observed while first walking normally and then on tiptoe, when the arch will appear in normal feet with flexible joints (Fig. 13.9). Neuromuscular defects are excluded by general examination and Gowers’ test. Incoordination abnormalities (which may be blamed on ‘flat feet’) are excluded by the child being able to hop on one leg.