Salter innominate osteotomy is an effective reconstructive
procedure for the treatment of developmental dysplasia of the hip
(DDH), but some children have a poor outcome at skeletal maturity.
In order to investigate factors associated with an unfavourable
outcome, we assessed the development of the contralateral hip. We retrospectively
reviewed 46 patients who underwent a unilateral Salter osteotomy
at between five and seven years of age, with a mean follow-up of
10.3 years (7 to 20). The patients were divided into three groups
according to the centre–edge angle (CEA) of the contralateral hip
at skeletal maturity: normal (>
25°, 22 patients), borderline (20°
to 25°, 17 patients) and dysplastic (<
20°, 7 patients). The
CEA of the affected hip was measured pre-operatively, at eight to
nine years of age, at 11 to 12 years of age and at skeletal maturity.
The CEA of the affected hip was significantly smaller in the borderline
and dysplastic groups at 11 and 12 years of age (p = 0.012) and
at skeletal maturity (p = 0.017) than in the normal group. Severin
group III was seen in two (11.8%) and four hips (57.1%) of the borderline
and dysplastic groups, respectively (p <
0.001). Limited individual development of the acetabulum was associated
with an unfavourable outcome following Salter osteotomy. Cite this article:
We reviewed 98 children (133 hips) with developmental dysplasia of the hip who underwent arthrography immediately after closed reduction by overhead traction. We followed the patients to skeletal maturity to investigate whether soft-tissue interposition influences acetabular development and avascular necrosis over the long term. The shape of the limbus and the thickness of the soft-tissue interposition at the acetabular floor, as shown on arthrograms at the time of reduction, were not directly related to the final radiological results or to the incidence of avascular necrosis. Even if marked soft-tissue interposition was found on the initial arthrogram, spontaneous disappearance was noted in 71% up to the age of five years. The final radiological results showed no difference between those in which the interposition disappeared and those with none at the time of closed reduction. However, the requirement for secondary surgery at the age of five years was significantly higher in those with more than 3.5 mm of soft-tissue interposition. In the no-disappearance group (group C) further operation was necessary in 100% and the results were significantly worse at maturity according to Severin’s classification. We suggest that the indications for open reduction should not be based solely on the arthrographic findings at the time of closed reduction.
We studied the morphological changes in the proximal femur in 42 patients (42 hips) who had had varus derotation osteotomy of the upper femur for residual acetabular dysplasia and congenital subluxation of the hip and who did not show deformity of the head of the femur. In 19 patients the alignment of the whole leg was examined. The femoral neck-shaft angle (FNSA) at the final examination was unrelated to that immediately after operation or to the state of the acetabulum at that time. The postoperative FNSA was not related to the final result but the CE angle obtained at surgery influenced the outcome. The femoral length did not differ significantly between the unaffected and affected sides. Significant differences were found in the femorotibial angle (176.6 degrees v 174.5 degrees) and in the point of intersection between the mechanical axis and knee (65.0% v 57.2%).
We reviewed the serial radiographs of 54 hips in 47 children treated by closed reduction for congenital dislocation of the hip and followed to at least 14 years of age, to determine the causes of acetabular dysplasia. We excluded hips with femoral head deformity or residual subluxation and compared the results with those from a control series of unaffected hips of patients with unilateral CDH. Acetabular development after the age of 11 or 12 years was significantly worse in Severin group III than in Severin group I hips on the affected side or Severin group III in unaffected control hips. One of the causes of acetabular dysplasia at maturity was found to be impairment of acetabular development after 11 or 12 years of age. This may be attributable to impaired secondary ossification in the acetabular rim. Our findings emphasise the importance of continuing the follow-up of patients treated for congenital dislocation of the hip until full skeletal maturity.
