We undertook a retrospective comparative study of all patients with an unstable slipped capital femoral epiphysis presenting to a single centre between 1998 and 2011. There were 45 patients (46 hips; mean age 12.6 years; 9 to 14); 16 hips underwent intracapsular cuneiform osteotomy and 30 underwent pinning in situ, with varying degrees of serendipitous reduction. No patient in the osteotomy group was lost to follow-up, which was undertaken at a mean of 28 months (11 to 48); four patients in the pinning in situ group were lost to follow-up, which occurred at a mean of 30 months (10 to 50). Avascular necrosis (AVN) occurred in four hips (25%) following osteotomy and in 11 (42%) following pinning in situ. AVN was not seen in five hips for which osteotomy was undertaken > 13 days after presentation. AVN occurred in four of ten (40%) hips undergoing emergency pinning in situ, compared with four of 15 (47%) undergoing non-emergency pinning. The rate of AVN was 67% (four of six) in those undergoing pinning on the second or third day after presentation.

Pinning in situ following complete reduction led to AVN in four out of five cases (80%). In comparison, pinning in situ following incomplete reduction led to AVN in 7 of 21 cases (33%). The rate of development of AVN was significantly higher following pinning in situ with complete reduction than following intracapsular osteotomy (p = 0.048). Complete reduction was more frequent in those treated by emergency pinning and was strongly associated with AVN (p = 0.005).

Non-emergency intracapsular osteotomy may have a protective effect on the epiphyseal vasculature and should be undertaken with a delay of at least two weeks. The place of emergency pinning in situ in these patients needs to be re-evaluated, possibly in favour of an emergency open procedure or delayed intracapsular osteotomy. Non-emergency pinning in situ should be undertaken after a delay of at least five days, with the greatest risk at two and three days after presentation. Intracapsular osteotomy should be undertaken after a delay of at least 14 days. In our experience, closed epiphyseal reduction is harmful.

Cite this article: Bone Joint J 2015;97-B:412–19.

We report the effect of introducing a dedicated Ponseti service on the five-year treatment outcomes of children with idiopathic clubfoot.

Between 2002 and 2004, 100 feet (66 children; 50 boys and 16 girls) were treated in a general paediatric orthopaedic clinic. Of these, 96 feet (96%) responded to initial casting, 85 requiring a tenotomy of the tendo-Achillis. Recurrent deformity occurred in 38 feet and was successfully treated in 22 by repeat casting and/or tenotomy and/or transfer of the tendon of tibialis anterior, The remaining 16 required an extensive surgical release.

Between 2005 and 2006, 72 feet (53 children; 33 boys and 20 girls) were treated in a dedicated multidisciplinary Ponseti clinic. All responded to initial casting: 60 feet (83.3%) required a tenotomy of the tendo-Achillis. Recurrent deformity developed in 14, 11 of which were successfully treated by repeat casting and/or tenotomy and/or transfer of the tendon of tibialis anterior. The other three required an extensive surgical release.

Statistical analysis showed that children treated in the dedicated Ponseti clinic had a lower rate of recurrence (p = 0.068) and a lower rate of surgical release (p = 0.01) than those treated in the general clinic.

This study shows that a dedicated Ponseti clinic, run by a well-trained multidisciplinary team, can improve the outcome of idiopathic clubfoot deformity.

Cite this article: Bone Joint J 2014;96-B:1424–6

Aim

To compare outcomes for children treated for idiopathic clubfeet with the Ponseti regimen before (2002–2004) and after (2005–2006) implementation of a dedicated Ponseti service.

Aim

10 years after the introduction of the Ponseti casting regimen as standard treatment for idiopathic clubfoot at Alder Hey Children's Hospital, we reviewed the mid-term outcomes of the initial 2-year cohort (treated from 2002–2004)

The association between idiopathic congenital talipes equinovarus (CTEV) and developmental dysplasia of the hip is uncertain. We present an observational cohort study spanning 6.5 years of selective ultrasound screening of hips in clubfoot. From 119 babies with CTEV there were nine cases of hip dysplasia, in seven individuals. This suggests that 1 in 17 babies with CTEV will have underlying hip dysplasia.

This study supports selective ultrasound screening of hips in infants with CTEV.

We report our initial experience of using the Ponseti method for the treatment of congenital idiopathic club foot.

Between November 2002 and November 2004 we treated 100 feet in 66 children by this method. The standard protocol described by Ponseti was used except that, when necessary, percutaneous tenotomy of tendo Achillis were performed under general anaesthesia in the operating theatre and not under local anaesthesia in the out-patient department. The Pirani score was used for assessment and the mean follow-up time was 18 months (6 to 30).

The results were also assessed in terms of the number of casts applied, the need for tenotomy of tendo Achillis and recurrence of the deformity. Tenotomy was required in 85 of the 100 feet. There was a failure to respond to the initial regimen in four feet which then required extensive soft-tissue release. Of the 96 feet which responded to initial casting, 31 (32%) had a recurrence, 16 of which were successfully treated by repeat casting and/or tenotomy and/or transfer of the tendon of tibialis anterior. The remaining 15 required extensive soft-tissue release. Poor compliance with the foot-abduction orthoses (Denis Browne splint) was thought to be the main cause of failure in these patients.

The practice of regular radiological follow-up of infants with a positive family history of developmental dysplasia of the hip is based on the widespread belief that primary acetabular dysplasia is a genetic disorder which can occur in the absence of frank subluxation or dislocation. We reviewed all infants who were involved in our screening programme for developmental dysplasia of the hip, between November 2002 and January 2004, and who had a normal clinical and ultrasound examination of the hip at six to eight weeks of age, but who, because of a family history of developmental dysplasia of the hip, had undergone further radiography after an interval of 6 to 12 months. The radiographs of 89 infants were analysed for signs of late dysplasia of the hip and assessed independently by three observers to allow for variability of measurement. There were 11 infants (11%) lost to follow-up.

All the patients had normal radiographs at the final follow-up and none required any intervention. We therefore question the need for routine radiological follow-up of infants with a positive family history of developmental dysplasia of the hip, but who are normal on clinical examination and assessment by ultrasound screening when six to eight weeks old.