Journal of Childrens Orthopaedics最新文献

Purpose: Non-surgical treatment is indicated in children with severe developmental dysplasia of the hip. Immobilisation may affect motor development. This study assessed motor outcomes in children treated with closed reduction, cast and brace or closed reduction and brace.

Methods: We conducted a retrospective study on 35 children (mean age 2.1 ± 1.4 months) and a prospective study on 17 children (mean age 1.4 ± 0.9 months), involving 68 hips (22 type D, 31 type III and 15 type IV). Treatment duration averaged 4.7 ± 2.2 months in retrospective study and 3.5 ± 1.9 months in prospective study. Multivariate regression analysed predictors of walking age, including treatment type, age at treatment start, developmental dysplasia of the hip severity, family history and breech presentation. A mixed-effects linear model compared treatment duration across studies. p values of z-score tests on regression coefficients are reported.

Results: Mean walking age was 14.6 ± 2.6 months in retrospective study and 14.7 ± 2.4 months in prospective study. Dysplasia severity (p < 0.05) and later treatment start (p < 0.001) predicted delayed walking age. Treatment type showed no overall effect; however, in type III, casts significantly delayed walking (p < 0.05). Severity had no impact when treatment began before 2 months, whereas later treatment led to significant differences based on severity (p < 0.01). At the last follow-up of prospective study, at 16 months, no parents reported persistent motor impairments compared with peers.

Conclusion: Treatment initiated within 2 months mitigates the effect of developmental dysplasia of the hip severity on motor development, resulting in similar walking outcomes across severities. These results underscore the importance of early treatment in severe developmental dysplasia of the hip.

Level of evidence: II.

Purpose: Objectives were to evaluate if gait was improved after multilevel surgery on the involved leg and simultaneously performed guided growth procedure on the uninvolved leg and whether simultaneously performed guided growth is efficient in limb length discrepancy management in hemiplegic children.

Methods: Gait pattern of 78 hemiplegic children (mean age 10.4 years) was evaluated using instrumented gait analysis before surgery and at 2 years. This study involved children with type 2a (Rodda and Graham classification) - 12, type 3 - 20, type 4 - 23, type 4s (undergone triceps lengthening at early age) - 23.

Results: The mean limb length discrepancy was 2.3 cm before surgery and 0.4 cm at final control. In all patients aged over 144 months, the residual length discrepancy was over 10 mm. The improvement in gait kinematics was observed on both the uninvolved and hemiplegic limbs. Finally, control on uninvolved leg kinematics presented values similar to reference values. On the involved leg, there were significant improvements in sagittal and transverse kinematics. Only patients of the 4s (patients undergone previous triceps lengthening surgery at an early age) group had no improvements in ankle flexion moment and power generation.

Conclusion: Multilevel surgery including simultaneous guided growth ensures improvements on both the uninvolved and hemiplegic limb gait kinematics. We suggest guided growth surgery before the age of 12 years for more exact equalization. Isolated triceps performed at an early age represent negative conditions for plantar flexion strength development in long term.

Introduction: Clubfoot is a congenital birth defect affecting musculoskeletal tissues of the affected lower legs, resulting in the typical appearance and changes in muscle-tendon properties. These properties change during development due to growth and activity, but how these properties differ across ages in clubfoot remains not fully understood. This study aimed to describe plantarflexor muscle-tendon volumes between affected and unaffected legs in unilateral clubfoot patients and explore the relationship between muscle volume and age.

Methods: A prospective cross-sectional study was performed on unilateral clubfoot patients treated with the Ponseti method. Muscle-tendon volumes of the medial and lateral gastrocnemius, soleus, and Achilles tendons in both affected and unaffected legs of clubfoot patients were assessed using ultrasound. Volumetric reconstructions were made using three-dimensional ultrasound (3DUS). Statistical analyses compared muscle-tendon volume between legs and their relationship with age.

Results: A total of 25 clubfoot patients with good clinical status aged between 2.0 and 11.8 years were analyzed. Smaller plantarflexor muscle and greater Achilles tendon volumes were found in the affected leg compared to the unaffected leg. Furthermore, age was not significantly related to absolute muscle volume difference between the legs.

Discussion and conclusions: The findings of this study indicate that changes in muscle and tendon volume are present in treated clubfoot patients of multiple ages, enhancing understanding of their muscle-tendon morphology. The clinical significance of muscle-tendon alterations and their adaptation to targeted interventions remains to be established. Further research should investigate the relationship between muscle-tendon morphology and clinical status of (relapsed) clubfoot patients.

Background: Beckwith-Wiedemann spectrum is a genetic disorder characterized by lateralized overgrowth, often presenting as limb bulk discrepancy. While limb-length discrepancies are documented in Beckwith-Wiedemann spectrum, the natural history of limb bulk discrepancy and hand/foot asymmetry progression remains less studied. This research examines limb bulk discrepancy progression in children with Beckwith-Wiedemann spectrum and identifies factors influencing its severity.

Methods: A retrospective, single-institution study analyzed 142 children with molecularly confirmed Beckwith-Wiedemann spectrum (imprinting center 2 loss of methylation, imprinting center 1 gain of methylation, and paternal uniparental isodisomy at chromosome 11). Limb measurements (upper arm, forearm, thigh, calf, palm, finger, and foot) were recorded during clinic visits. Linear mixed-effects models assessed relationships between genotype, age, limb bulk discrepancy progression, body mass index, and sex.

Results: The cohort included 90 imprinting center 2 loss of methylation, 41 paternal uniparental isodisomy at chromosome 11, and 11 imprinting center 1 gain of methylation patients. In the imprinting center 2 loss of methylation group, significant limb bulk discrepancy progression occurred in the upper arm (0.47 mm/year), calf (0.53 mm/year), and foot anterior-posterior dimension (0.40 mm/year; all p < 0.01). The paternal uniparental isodisomy at chromosome 11 genotype showed greater asymmetry in most regions compared to others (p < 0.01), except the middle finger. Asymmetry progression rates were similar across genotypes. Body mass index positively correlated with increased limb bulk discrepancy in the upper arm and calf.

Conclusions: Limb asymmetry in Beckwith-Wiedemann spectrum progresses slowly in specific regions, with genotype and body mass index influencing baseline severity. Patients with paternal uniparental isodisomy at chromosome 11 exhibit greater baseline limb bulk discrepancy, but progression rates are consistent across genotypes, highlighting the need for further research into lateralized overgrowth mechanisms and clinical implications.

Level of evidence: 3-Retrospective cohort study.