Aims

The aim of this study was to establish the incidence of developmental dysplasia of the hip (DDH) diagnosed after one-year of age in England, stratified by age, gender, year, and region of diagnosis.

Between June 1988 and December 1997, we treated 332 babies with 546 dysplastic hips in a Pavlik harness for primary developmental dysplasia of the hip as detected by the selective screening programme in Southampton. Each was managed by a strict protocol including ultrasonic monitoring of treatment in the harness. The group was prospectively studied during a mean period of 6.5 ± 2.7 years with follow-up of 89.9%. The acetabular index (AI) and centre-edge angle of Wiberg (CEA) were measured on annual radiographs to determine the development of the hip after treatment and were compared with published normal values.

The harness failed to reduce 18 hips in 16 patients (15.2% of dislocations, 3.3% of DDH). These required surgical treatment. The development of those hips which were successfully treated in the harness showed no significant difference from the normal values of the AI for the left hips of girls after 18 months of age. Of those dysplastic hips which were successfully reduced in the harness, 2.4% showed persistent significant late dysplasia (CEA < 20°) and 0.2% persistent severe late dysplasia (CEA < 15°). All could be identified by an abnormal CEA (< 20°) at five years of age, and many from the progression of the AI by 18 months. Dysplasia was considered to be sufficient to require innominate osteotomy in five (0.9%). Avascular necrosis was noted in 1% of hips treated in the harness.

We conclude that, using our protocol, successful initial treatment of DDH with the Pavlik harness appears to restore the natural development of the hip to normal. We suggest that regular radiological surveillance up to five years of age is a safe and effective practice.

We reviewed the management of 100 cases of slipped upper femoral epiphysis treated over a period of 26 years. A total of 14 slips was identified as unstable on admission. These underwent reduction and stabilisation within 24 hours of the onset of severe symptoms. Of the 86 stable slips four progressed to avascular necrosis (AVN), which was not seen in the unstable slips. The literature on slipped upper femoral epiphysis suggests that the acute unstable slip is at higher risk of developing AVN. We recommend reduction and stabilisation of unstable slips within 24 hours of the onset of symptoms in order to reduce the risk of AVN.

Between 1988 and 1995, we studied 91 club feet from a series of 120 recalcitrant feet in 86 patients requiring surgical treatment. There were 48 boys and 20 girls. The mean age at operation was 8.9 months. Surgery consisted of an initial plantar medial release followed two weeks later by a posterolateral release. This strategy was adopted specifically to address the problems of wound healing associated with single-stage surgery and to ascertain the rate of relapse after a two-stage procedure. Immobilisation in plaster was used for three months followed by night splintage. The feet were classified preoperatively and prospectively into four grades according to the system suggested by Dimeglio et al. Grade-1 feet were postural and did not require surgery. All wounds were closed primarily. One superficial wound infection occurred in a grade-4 foot and there were no cases of wound breakdown. The rate of relapse was 20.4% in grade-3 and 65.4% in grade-4 feet.

Two-stage surgery for the treatment of club foot seems to be effective in the reduction of wound problems but does not appear to give significantly better results in terms of relapse when performed for more severe deformities.

Chondrocytes at the lower zone of the growth plate must be eliminated to facilitate longitudinal growth; this is generally assumed to involve apoptosis. We attempted to provide definitive electron-microscopic evidence of apoptosis in chondrocytes of physes and chondroepiphyses in the rabbit. We were, however, unable to find a single chondrocyte with the ultrastructure of ‘classical’ apoptosis in vivo, although such a cell was found in vitro. Instead, condensed chondrocytes had a convoluted nucleus with patchy chromatin condensations while the cytoplasm was dark with excessive amounts of endoplasmic reticulum. These cells were termed ‘dark chondrocytes’. A detailed study of their ultrastructure combined with localisation methods in situ suggested a different mechanism of programmed cell death. In addition, another type of death was identified among the immature chondrocytes of the chondroepiphysis. These cells had the same nucleus as dark chondrocytes, but the lumen of the endoplasmic reticulum had expanded to fill the entire non-nuclear space, and all cytoplasm and organelles had been reduced to dark, worm-like inclusions. Since these cells appeared to be ‘in limbo’, they were termed ‘paralysed’ cells. It is proposed that ‘dark chondrocytes’ and ‘paralysed cells’ are examples of physiological cell death which does not involve apoptosis. It is possible that the confinement of chondrocytes within their lacunae, which would prevent phagocytosis of apoptotic bodies, necessitates different mechanisms of elimination.

We performed an audit of 71 children with consecutive displaced, extension-type supracondylar fractures of the humerus over a period of 30 months. The fractures were classified according to the Wilkins modification of the Gartland system. There were 29 type IIA, 22 type IIB and 20 type III. We assessed the effectiveness of guidelines proposed after a previous four-year review of 83 supracondylar fractures. These recommended that: 1) an experienced surgeon should be responsible for the initial management; 2) closed or open reduction of type-IIB and type-III fractures must be supplemented by stabilisation with Kirschner (K-) wires; and 3) K-wires of adequate thickness (1.6 mm) must be used in a crossed configuration.

The guidelines were followed in 52 of the 71 cases. When they were observed there were no reoperations and no malunion. In 19 children in whom they had not been observed more than one-third required further operation and six had a varus deformity. Failure to institute treatment according to the guidelines led to an unsatisfactory result in 11 patients. When they were followed the result of treatment was much better. We have devised a protocol for the management of these difficult injuries.

We report the six-year results of a prospective, controlled demographic trial of developmental dysplasia of the hip (DDH) treated in the Pavlik harness using ultrasound supervision. Our aim was to assess the value of ultrasound and its role in monitoring reduction in the harness, in terms of progression or failure of reduction at an early state.

From 1988 to 1994, a total of 221 patients with 370 ultrasonographically abnormal hips was treated in the Pavlik harness. This represents a treatment rate for the Southampton district of 5.1 per 1000 live births. Sixteen hips in 12 patients were not reduced in the harness and required surgical treatment; 95.7% were successfully reduced. One case of mild avascular necrosis (0.3%) was identified in those treated by harness alone. Of the 221 patients 87.8% remain under radiological review, with 3.2% of affected hips showing continued, mild acetabular dysplasia.

We conclude that ultrasound monitoring has led to an acceptably low level of intervention, a high reduction rate and minimal iatrogenic complications. The trial is continuing.

Only two cases have been reported of congenital dislocation of the hip in infants born after extrauterine pregnancies. We report a further two and discuss the management and the variable outcome. These cases seem to confirm that congenital dislocation of the hip is associated with moulding forces rather than being a teratological abnormality.

We report a series of 15 children, six male and nine female, of average age 20 months, seen at a paediatric orthopaedic clinic with torticollis. Orthopaedic examination revealed a normal range of neck movement in all cases but in seven there was palpable tightness in the absence of true shortening or contracture of the sternomastoid muscle.

The patients were prospectively referred for ocular examination. In five of the 15 an ocular cause for the torticollis was detected with underaction of the superior oblique muscle in three, paresis of the lateral rectus muscle in one and nystagmus in one. Another two patients were found to have an abnormal ocular examination which was thought to be unrelated to their torticollis. Three of the patients with ocular torticollis required extra-ocular muscle surgery to abolish the head tilt and one of these had a tight sternomastoid muscle. Two of the non-ocular group had surgical release of the sternomastoid muscle; in the rest, the condition either resolved with physiotherapy or required no active treatment.

We recommend that all patients with torticollis and no clear orthopaedic cause are referred for ocular assessment since it is not possible clinically to distinguish ocular from non-ocular causes.