Equinovarus
Benjamin Joseph, Selvadurai Nayagam, Randall Loder, Ian Torode in Paediatric Orthopaedics, 2016
In congenital clubfoot, genetic, foetal and intrauterine ‘packaging’ issues and neuromuscular conditions are thought to be involved in causation. There are higher risks if the child is male, born to a primiparous mother and there is a positive family history in a first degree relative (20–30 times more likely). Some pregnancy-related conditions also increase risk, for example, early amniocentesis, issues around foetal constraint (oligohydramnios, breech delivery) and mothers with a high BMI.2 The association with hip dysplasia is now refuted but a first assessment of the child with a congenital clubfoot should include a check for spinal problems or other joint contractures as in multiple congenital contractures (arthrogryposis).3 In the absence of an identifiable cause, the clubfoot is idiopathic; this is the case for the majority of cases. Approximately half the cases have both feet affected.
Evidence-Based Medicine in Low- and Middle-Income Countries
Alaaeldin (Alaa) Azmi Ahmad, Aakash Agarwal in Early-Onset Scoliosis, 2021
While orthopaedic trauma literature has largely been a prime focus among emerging EBM publications focussing on LMICs, little is known about common paediatric pathologies and their management in these countries. Owen et al. [14] attempted to provide some global perspective to clubfoot management in LMICs. Clubfoot occurs in an estimated incidence of 1.24/1000 live births, affecting upwards of 174,000 children born annually, with approximately 90% of these children born in LMICs [14]. Untreated, clubfoot has lifelong impairment, deformity, and long-term consequences on overall health and function. With a primarily nonsurgical approach adopted globally after the popularisation of the Ponseti serial casting method, Owen et al. [14] reported on the difficulties of incorporating such a care practise to LMICs. A cross-sectional survey of clinicians treating clubfoot was conducted with respondents from 55 countries comprising an estimated coverage of nations with up to 79% of predicted clubfoot cases. Compiled responses revealed low coverage for these patients with less than 15% of children born with clubfoot in LMICs receiving treatment [14]. Importantly, however, the authors noted that responses indicate increased coverage since 2005 when Ponseti treatment became more widely known and accepted. The importance of early intervention to prevent or diminish lifelong deformity and functional impairment in these patients cannot be overstated. With an understanding of the difficulties of quantifying the burden of orthopaedic pathology in LMICs and trying to establish an understanding of the type of care being provided, we can now begin to better understand the difficulties with approaching evidence-based spine care in LMICs with a focus on the paediatric spine.
Epidemiology of clubfoot
R. L. Mittal in Clubfoot, 2018
It is the most common foot deformity in which the foot is plantar flexed, adducted, and inverted, whereas varus obviously stands for both adduction and inversion. These three components of the deformity are present in varying proportions of severity and rigidity. However, there is a fourth component of deformity also, that is, cavus, invariably present in varying severity and rigidity, but in the nomenclature (equinovarus), it does not find a place. To be exact, it should be called equino-cavo-varus, but by convention, it is called equinovarus only. This is an anomalous situation, cavus being an important component of composite deformity and remaining neglected by name. This component of the deformity also requires correction in order to achieve a good functional and cosmetic result. In this book, this has been handled with a new perspective in Chapter 4, which also discusses its pathoanatomy. There is yet another omission in the nomenclature. Among its various types, idiopathic variety is by far the most common type, from very mild to the most severe. Technically, it should be known as idiopathic congenital clubfoot, being present since birth and of unknown etiology. However, it is simply called clubfoot, and it has continued to be named as such since ancient times, being a short and simple name. When we say clubfoot, it means idiopathic; all others have to be addressed along with their cause. There is a tremendous variation in the deformity from case to case, and each clubfoot is different with regard to severity and rigidity. The equinus deformity, viewed in a different perspective, has been a significant part of research by the author and is discussed in detail in Chapter 4, proving its veracity on numerous evidences. This is a highly important fact, taken care of in the treatment of extreme clubfoot deformities.
Timing for Ponseti clubfoot management: does the age matter? 90 children (131 feet) with a mean follow-up of 5 years
Published in Acta Orthopaedica, 2018
Yu-Bin Liu, Song-Jian Li, Li Zhao, Bo Yu, Da-Hang Zhao
The proposal that congenital clubfoot should be treated soon after birth has been widely accepted (Dobbs et al. 2004, Morcuende et al. 2004, Dobbs and Gurnett 2009, Zhao et al. 2014a, Liu et al. 2016). Ponseti (1996) also suggested that initial treatment should begin in the first few weeks of life to take advantage of the more favorable viscoelastic properties of the connective tissues in the newborn. The upper limit age for Ponseti method management is unclear. Several authors have reported that neglected clubfoot cases or patients presenting at an older age could also be successfully managed by the Ponseti method (Lourenco and Morcuende 2007, Spiegel et al. 2009, Khan and Kumar 2010, Ayana et al. 2014). In a recently published study in which 11 neglected patients with a mean age of 11 years (6–19) were treated with a modified Ponseti method, 17 out of 18 feet achieved a good result with no need for further surgery (Haj Zargar Bashi et al. 2016). It is still unknown whether the age at initiation of treatment influences the clinical outcome and the rate of relapse.
Prenatal sonographic findings in a cohort of foetuses with a confirmed 22q11.2 microdeletion at a single Chinese Tertiary Centre
Published in Journal of Obstetrics and Gynaecology, 2022
Xiang-Yi Jing, Yong-Ling Zhang, Li Zhen, Yan-Lin Li, Dong-Zhi Li
For extracardiac anomalies, multicystic dysplastic kidney and clubfoot were the two most common findings in our series. In postnatal cases, genitourinary tract abnormalities have been reported to be present in 30–40% of del22q11.2 patients, and findings of hydronephrosis, unilateral renal agenesis, and multicystic dysplastic kidney occur at higher rates than expected in the general population (Van Batavia et al. 2019). Clubfoot was the only skeletal system anomaly identified in our series, and was found in 5 cases and as a single finding in 2 cases. One study reported with 1,466 patients that the prevalence of clubfoot in del22q11.2 is 30 times higher than that observed in the general population, and suggested that the diagnosis of clubfoot, especially in combination with other typically associated abnormalities of 22q11.2DS, should provoke consideration of this condition as an underlying diagnosis (Homans 2018).
FEVR findings in patients with Loeys-Dietz syndrome type II
Published in Ophthalmic Genetics, 2018
Mark A. Solinski, Michael P. Blair, Harry Dietz, David Mittelman, Michael J. Shapiro
His past medical history was notable for a prenatal diagnosis of bilateral clubfoot and a dilated and tortuous aorta on maternal ultrasound. He was born after a full term of gestation. After birth, the patient showed cleft palate and bilateral finger contractures. MRI revealed dilated anterior part of the lateral ventricle. Ultrasound revealed dilated extrarenal pelvis. Echocardiogram noted patent ductus arteriosus, patent foramen ovale, and spontaneous pneumothorax. The aortic root diameter measured 2.4 cm (z-score of 3.77). Further examination showed exotropia, lumbar kyphosis, crumpled ears, frontal bossing, bifid uvula with cleft soft palate, slight retrognathia, lateral deviation of the fingers, mild adduction of the feet, dolichocephaly, craniosynostosis, malar hypoplasia, orbital hypertelorism, widely spaced teeth, arachnodactyly, translucent skin, pes planus, increased elbow extension, and basilar invagination with C2-C3 instability. His height charted at the 95th percentile. The clinical diagnosis of LDS was established on the basis of the skin findings, skeletal and craniofacial features, and aortic root dilation. At 8 months, genetic analysis found a mutation in TGFBR2 (p. R528H) and confirmed LDS Type II. Parental testing showed the mutation was acquired de novo. Surgical interventions included aortic root replacement at 9 months, strabismus surgery at 14 months old, cleft palate repair at 17 months, and a second aortic root replacement with valve replacement at 9 years.
Related Knowledge Centers
- Arthrogryposis
- Birth Defect
- Ultrasound
- Connective Tissue
- Contracture
- Skeletal Muscle
- Idiopathic Disease
- Twin
- Spina Bifida
- Ponseti Method