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Avascular necrosis in congenital hip dislocation. The significance of splintage
Insights
Avascular necrosis (AVN) is a complication of hip dislocation treatment. This study found AVN incidence was low with the Denis Browne splint alone, but higher when combined with manipulation and plaster casts.
Area of Science:
- Orthopedics
- Pediatric Orthopedics
- Skeletal Dysplasias
Background:
- Avascular necrosis (AVN) is a known complication in treating congenital hip dislocation.
- The modified Denis Browne splint is a common treatment modality.
Purpose of the Study:
- To assess the incidence of avascular necrosis and other complications in children treated with the modified Denis Browne splint.
- To determine the specific contribution of the splint versus other treatment components to AVN development.
Main Methods:
- Retrospective review of 211 children treated with the modified Denis Browne splint.
- Analysis of complications, specifically avascular necrosis, based on treatment protocol (splint alone, splint with tenotomy and plaster, etc.).
Main Results:
- Six of 238 hips (2.5%) treated with the splint alone developed radiographic avascular necrosis.
- Twenty of 33 hips (60.6%) treated with tenotomy, plaster spica, and splint showed radiographic AVN.
- Overall significant long-term growth disturbance occurred in 0.7% of cases.
Conclusions:
- The modified Denis Browne splint alone has a low incidence of causing avascular necrosis.
- Manipulation and plaster casting, rather than the splint itself, are the primary contributors to avascular necrosis in this treatment context.
Abstract:
Avascular necrosis is an iatrogenic complication of the treatment of congenital dislocation of the hip. In order to assess the incidence of this and other complications, we have reviewed a consecutive series of 211 children treated at some stage with the modified Denis Browne splint used in Adelaide. In 173 children treated with this splint alone for 238 subluxed or dislocated hips which were stable when reduced, six hips (2.5%) developed radiographic avascular necrosis, though there was progressive growth deformity in only one. There was a much higher incidence among cases treated for unstable reduction by tenotomy, plaster spica and then the splint, 20 of 33 hips (60.6%) showing radiographic signs, though only one led to progressive abnormality. Of seven patients treated by adductor tenotomy and the splint no case of avascular necrosis was encountered. In the whole series the incidence of significant long-term growth disturbance in children treated in this splint was 0.7%. The great majority of our cases of avascular necrosis were attributable to manipulation and plaster, not to the subsequent use of a splint.