Genu Valgum in Children: Diagnostic and Therapeutic Alternatives

Total Page:16

File Type:pdf, Size:1020Kb

Genu Valgum in Children: Diagnostic and Therapeutic Alternatives Genu Valgum in Children: Diagnostic and Therapeutic Alternatives Gregory R. White, MD, and Gregory A. Mencio, MD Abstract Genu valgum is a common orthopaedic problem in children. The vast majority femoral anteversion and compen- of cases are physiologic variants, which resolve normally. However, there are satory external tibial torsion may pathologic entities due to both focal and systemic processes in which the defor- have the appearance of valgus mity often progresses and usually requires treatment. Differentiating between malalignment of the knee when, in the two forms is facilitated by a thorough understanding of the natural history of fact, no frontal-plane deformity the development of the tibiofemoral angle in children. In this review, an approach exists. The appearance of genu val- to the evaluation and diagnosis of genu valgum is presented, and therapeutic gum in this situation is due to alternatives are discussed. malalignment in the transverse J Am Acad Orthop Surg 1995;3:275-283 (rotational) plane. Pathologic Genu Valgum Genu valgum, or knock-knee, is a and 22 months and progresses into Pathologic genu valgum is much common condition affecting the maximum valgus angulation (10 to less common than the physiologic lower limbs in children and adoles- 15 degrees) at around 3 years of age. type. However, numerous causes cents that the orthopaedist is often The normal child then has a gradual exist. Both focal and systemic called on to evaluate. As with genu resolution to physiologic knee val- processes may cause deformity that varum, physiologic forms are most gus (7 to 8 degrees) over the ensuing either is localized to a specific site common; however, pathologic years (Fig. 1). Using clinical tech- within the bone or is more general- causes, which have the propensity to niques of measurement, Staheli et ized, involving the whole bone. By progress and may require treatment, al2,3 have reported a similar pattern definition, children with pathologic do exist (Table 1). It is obviously of development. genu valgum have tibiofemoral important to distinguish between In the vast majority of children angles that are outside two standard these entities. In this review, we will with genu valgum, the tibiofemoral deviations of the mean.1-3 This mea- present an approach to the evalua- angle is within the physiologic surement varies as a function of age tion, diagnosis, and treatment of range of two standard deviations genu valgum in children. above or below the mean. They can be treated with observation and parental reassurance that the Dr. White is Chief Resident, Department of Orthopaedics and Rehabilitation, Vanderbilt Physiologic Genu Valgum “deformity” is a variant of normal University Medical Center, Nashville, Tenn. 1-3 and not a disease. Staheli has Dr. Mencio is Assistant Professor, Department Evaluating angular malalignment is suggested that such children are of Orthopaedics, Vanderbilt University School of simplified if one is familiar with the probably best described as having Medicine, Nashville. normal development of the tibio- knock-knees.2 Fat thighs, ligamen- femoral angle. Salenius and Vankka1 tous laxity, and flatfoot, which often Reprint requests: Dr. Mencio, Department of Orthopaedics and Rehabilitation, Vanderbilt have shown in a radiographic study results in toed-out habitus, can University Medical Center, Nashville, TN that the tibiofemoral angle in the accentuate the knock-kneed appear- 37232-2550. newborn is characterized by maxi- ance4 and cause physiologic genu mal lateral bowing (genu varum valgum to seem more severe. Tor- Copyright 1995 by the American Academy of angulation of 10 to 15 degrees). It sional malalignment can have a sim- Orthopaedic Surgeons. straightens between the ages of 20 ilar effect. Children with excessive Vol 3, No 5, September/October 1995 275 Genu Valgum in Children equate reduction or physeal injury gressive angular deformity.6 These Table 1 and subsequent growth arrest. In injuries should be looked for dili- Classification of Genu Valgum the proximal tibia, as in other parts gently, and families should be of the immature skeleton, Salter- informed of the potential conse- Physiologic Knock-knees Harris type III, IV, and V fractures quences to avoid subsequent Apparent genu valgum (fat pose the greatest risk of this occur- embarrassment, misunderstand- thighs, rotational deformity) rence. In contrast, several authors ing, and potential liability. Hresko Pathologic have shown that in the distal femur and Kasser6 recommend that all Idiopathic the fracture type is not predictive of patients with traumatic injury to Unresolved physiologic valgus future growth problems.5 Due to the lower extremity undergo radio- Lateral femoral hypoplasia the large cross-sectional area and graphic evaluation of the knee in Posttraumatic the convoluted anatomy of this addition to a thorough clinical eval- Malunion growth plate, damage to the physeal uation. Physeal arrest cartilage is probably extensive Another common cause of genu Metaphyseal tibial fracture despite the pattern of injury. Fur- valgum is tibia valga following Metabolic Rickets thermore, the geometry of this fracture of the proximal tibial me- Renal osteodystrophy physis may affect the ability to taphysis (Fig. 3). Since the first Neuromuscular achieve an adequate, anatomic description by Cozen7 in 1953, there Cerebral palsy reduction. have been many reports of this Paralytic conditions (e.g., It is worth mentioning that problem. Hosts of possible theories poliomyelitis) occult physeal injuries to the knee about etiology have been proposed, Infectious (e.g., osteomyelitis) may occur concomitantly with although the actual cause of the Generalized disorders more overt fractures of the metaph- abnormality remains unknown. Juvenile arthritis yseal and diaphyseal regions of the Cozen suggested that the problem Osteochondrodysplasia tibia and femur and can lead to pro- was due to asymmetric stimulation Osteogenesis imperfecta (Fig. 1). Deformity is more apt to be +20° unilateral, and treatment is often necessary. +15° Idiopathic Varus +10° Idiopathic genu valgum occurs when physiologic variants fail to +5° resolve, leading to persistent or pro- gressive deformity. Children with 0° this diagnosis are often obese and flatfooted and characterized by liga- -5° mentous laxity.4 Hypoplasia of the lateral femoral condyle and stretch- Valgus -10° ing of the medial soft-tissue struc- tures of the knee may develop in response to prolonged, excessive -15° weight-bearing through the lateral half of the joint (Fig. 2). 1 2 345 6 7891011 12 13 Age, yr Posttraumatic Trauma is probably the most Fig. 1 Graph illustrating the development of the tibiofemoral angle in children during growth, based on measurements from 1,480 examinations of 979 children. Of the lighter common cause of pathologic genu lines, the middle one represents the mean value at a given point in time, and the other two valgum. Fractures of the distal represent the deviation from the mean. The darker line represents the general trend. femur or proximal tibia can lead to (Adapted with permission from Salenius P, Vankka E: The development of the tibiofemoral angle in children. J Bone Joint Surg Am 1975;57:259-261.) valgus deformity due to either inad- 276 Journal of the American Academy of Orthopaedic Surgeons Gregory R. White, MD, and Gregory A. Mencio, MD and postulated that medial soft-tis- sue interposition was the cause of the deformity. More recently, Jordan et al13 reported on seven patients with this deformity, reviewed the major theo- ries regarding the etiology of this problem, and concluded that the most likely primary mechanism is growth stimulation of the medial portion of the proximal tibia due to fracture hyperemia. This is cur- rently the prevailing theory and is strongly supported by the findings in two case reports. Green14 re- ported a case of posttraumatic tibia valga in which the mechanism of medial overgrowth of the proximal tibia was supported by the finding of asymmetric growth-arrest lines. Zionts et al15 reported a case of tibia A B valga that showed increased radionuclide activity in the medial half of the proximal tibial growth plate on a bone scan. Metabolic Metabolic causes of pathologic Fig. 2 Idiopathic genu valgum in an obese genu valgum include the various teenager in whom physiologic valgus failed forms of rickets and renal osteodys- to resolve. Note the asymmetric involve- ment (greater on the left) and the hypoplasia trophy. Although the metabolic of the lateral femoral condyle, suggesting effects on the physis are similar in excessive lateral loading. these disorders, vitamin D–resistant and vitamin D–deficient rickets are more typically associated with varus deformity at the knee, and of the proximal tibial physis.8 Tay- renal osteodystrophy is typically lor9 attributed it to overgrowth of associated with valgus deformity.16 the tibia relative to the fibula. This difference is thought to be Salter and Best10 felt that mal- related to the pattern of mechanical union was the most important fac- loading of the physes as determined tor in the pathogenesis of the by the alignment of the knee at the valgus angulation. Houghton and time the metabolic process mani- Rooker11 experimentally produced fests itself.17 tibia valga in rabbits by sectioning Most of the disorders that are the pes anserinus and medial responsible for vitamin D–resistant C periosteum and postulated a teth- and vitamin D–deficient rickets are present from birth. Therefore, the ering
Recommended publications
  • Genu Varum and Genu Valgum Genu Varum and Genu Valgum
    Common Pediatric Lower Limb Disorders Dr.Kholoud Al-Zain Assistant Professor Consultant, Pediatric Orthopedic Surgeon Nov- 2018 Acknowledgement: Dr.Abdalmonem Alsiddiky Dr.Khalid Bakarman Prof. M. Zamzam Topics to Cover 1. In-toeing 2. Genu (varus & valgus), & proximal tibia vara 3. Club foot 4. L.L deformities in C.P patients 5. Limping & leg length inequality 6. Leg aches 1) Intoeing Intoeing- Evaluation • Detailed history – Onset, who noticed it, progression – Fall a lot – How sits on the ground • Screening examination (head to toe) • Pathology at the level of: – Femoral anteversion – Tibial torsion – Forefoot adduction – Wandering big toe Intoeing- Asses rotational profile Pathology Level Special Test • Femoral anteversion • Hips rotational profile: – Supine – Prone • Tibial torsion • Inter-malleolus axis: – Supine – Prone • Foot thigh axis • Forefoot adduction • Heel bisector line • Wandering big toe Intoeing- Special Test Foot Propagation Angle → normal is (-10°) to (+15°) Intoeing- Femoral Anteversion Hips rotational profile, supine → IR/ER normal = 40-45/45-50° Intoeing- Tibial Torsion Inter-malleolus axis Supine position Sitting position Intoeing- Tibial Torsion Foot Thigh Axis → normal (0°) to (-10°) Intoeing- Forefoot Adduction Heel bisector line → normal along 2 toe Intoeing- Adducted Big Toe Intoeing- Treatment • Establish correct diagnosis • Parents education • Annual clinic F/U → asses degree of deformity • Femoral anti-version → sit cross legged • Tibial torsion → spontaneous improvement • Forefoot adduction → anti-version
    [Show full text]
  • Pierre Robin and the Syndrome That Bears His Name PETER RANDALL
    Pierre Robin and the Syndrome That Bears His Name PETER RANDALL, M.D. WILTON M. KROGMAN, Ph.D. SOONA JAHINA, B.D.S., M.Sc. Philadelphia, Pennsylvania The Pierre Robin Syndrome refers to a combination of micrognathia (a small jaw) and glossoptosis (literally, a falling downward or back- ward of the tongue) in the newborn infant (Figure 1). These conditions are likely to cause obstruction of the upper airway, and they are fre- quently associated with an incomplete cleft of the palate. Patients with the Pierre Robin Syndrome may present a real emer- gency in the delivery room because of the obstructed upper airway, or the airway problem may not become manifest for several days or weeks (10, 11, 38). There is frequently a feeding problem, as well as problems associated with the cleft of the palate (if one is present) and also an unusual malocclusion (2, 5, 12, 16). In addition, it presents a fascinating anthropological puzzle (22, 23). This paper will review the work of Dr. Robin, consider some possible etiologies of this syndrome, and report on some work on mandibular bone growth in a group of such patients. History Pierre Robin was far from the first person to recognize this syndrome. One account is recorded in 1822 by St. Hilaire. In 1891 Taruffi men- tioned two subclassifications-hypomicrognatus (small jaw) and hypo- agnathus (absent jaw). In 1891, four cases, two of them having cleft palates, were reported by Lanneloague and Monard (12, 14). Shukow- sky in 1902 described a tongue to lip surgical adhesion to overcome the respiratory obstruction (34).
    [Show full text]
  • Peds Ortho: What Is Normal, What Is Not, and When to Refer
    Peds Ortho: What is normal, what is not, and when to refer Future of Pedatrics June 10, 2015 Matthew E. Oetgen Benjamin D. Martin Division of Orthopaedic Surgery AGENDA • Definitions • Lower Extremity Deformity • Spinal Alignment • Back Pain LOWER EXTREMITY ALIGNMENT DEFINITIONS coxa = hip genu = knee cubitus = elbow pes = foot varus valgus “bow-legged” “knock-knee” apex away from midline apex toward midline normal varus hip (coxa vara) varus humerus valgus ankle valgus hip (coxa valga) Genu varum (bow-legged) Genu valgum (knock knee) bow legs and in toeing often together Normal Limb alignment NORMAL < 2 yo physiologic = reassurance, reevaluate @ 2 yo Bow legged 7° knock knee normal Knock knee physiologic = reassurance, reevaluate in future 4 yo abnormal 10 13 yo abnormal + pain 11 Follow-up is essential! 12 Intoeing 1. Femoral anteversion 2. Tibial torsion 3. Metatarsus adductus MOST LIKELY PHYSIOLOGIC AND WILL RESOLVE! BRACES ARE HISTORY! Femoral Anteversion “W” sitters Internal rotation >> External rotation knee caps point in MOST LIKELY PHYSIOLOGIC AND MAY RESOLVE! Internal Tibial Torsion Thigh foot angle MOST LIKELY PHYSIOLOGIC AND WILL RESOLVE BY SCHOOL AGE Foot is rotated inward Internal Tibial Torsion (Fuchs 1996) Metatarsus Adductus • Flexible = correctible • Observe vs. casting CURVED LATERAL BORDER toes point in NOT TO BE CONFUSED WITH… Clubfoot talipes equinovarus adductus internal varus rotation equinus CAN’T DORSIFLEX cavus Clubfoot START19 CASTING JUST AFTER BIRTH Calcaneovalgus Foot • Intrauterine positioning • Resolve
    [Show full text]
  • Association of Mutations in FLNA with Craniosynostosis
    European Journal of Human Genetics (2015) 23, 1684–1688 & 2015 Macmillan Publishers Limited All rights reserved 1018-4813/15 www.nature.com/ejhg ARTICLE Association of mutations in FLNA with craniosynostosis Nathalie Fennell1, Nicola Foulds2,3, Diana S Johnson4, Louise C Wilson5, Michelle Wyatt6, Stephen P Robertson7, David Johnson1, Steven A Wall1 and Andrew OM Wilkie*,1,8 Mutations of FLNA, an X-linked gene that encodes the cytoskeletal protein filamin A, cause diverse and distinct phenotypes including periventricular nodular heterotopia and otopalatodigital spectrum disorders (OPDS). Craniofacial abnormalities associated with OPDS include supraorbital hyperostosis, down-slanting palpebral fissures and micrognathia; craniosynostosis was previously described in association with FLNA mutations in two individual case reports. Here we present four further OPDS subjects who have pathological FLNA variants and craniosynostosis, supporting a causal link. Together with the previously reported patients, frontometaphyseal dysplasia was the most common clinical diagnosis (four of six cases overall); five patients had multiple suture synostosis with the sagittal suture being the most frequently involved (also five patients). No genotype– phenotype correlation was evident in the distribution of FLNA mutations. This report highlights the need to consider a filaminopathy in the differential diagnosis of craniosynostosis, especially in the presence of atypical cranial or skeletal features. European Journal of Human Genetics (2015) 23, 1684–1688; doi:10.1038/ejhg.2015.31; published online 15 April 2015 INTRODUCTION stenosis, and ureteric and urethral stenosis.9 Melnick–Needles syn- The phenotypic spectrum associated with mutations in FLNA is drome (MNS) is usually lethal in males; facial features in affected unusually diverse and correlates with the functional consequence for females include prominent supraorbital ridge, exorbitism, oligohypo- the filamin A protein.
    [Show full text]
  • Promising: Process Improvement in Psychosocial Health
    PROMISing: Process Improvement in Psychosocial Health Carly Woodmark MS │ Dereesa Reid MBA │ Daniel Bouton MD SHC-Portland │ Department of Performance Improvement Abstract no. 20 Shriners Team And Patients PROMISing Changes Shriners Hospitals for Children is a network of 22 non-profit medical facilities across North America. Benefits of PROMIS Intervention Pre-op Post-op Since 1924, SHC-Portland has treated a wide range of pediatric orthopedic conditions, from fractures to rare diseases and syndromes. Our Integrated Practice Unit of multi-disciplinary Minor burden of taking PROMIS is offset by quality professionals provide a comprehensive approach through specialized evaluation and treatment communication of meaningful progress between along with rehabilitative services to restore each child physically, emotionally, and socially. Below is patient/family & physician during clinic visit. a list of common conditions treated at SHC-Portland. Medical providers can demonstrate improvements Skeletal abnormalities – Osteogenesis imperfecta (OI), osteochondritis dissecans (OCD lesions), from interventions & adjust care management if Blount disease, skeletal dysplasias, etc. needed. Outcome Performance Improvement Neuromuscular conditions – Cerebral palsy, myelomeningocele (spina bifida), Muscular dystrophy, spinal muscular atrophy After one year of data collection, rates of Minimal Clinical Important Difference (MCID) were assessed for all patient-reported domains in both surgical and non-surgical populations. Multivariate Hand/Upper extremity
    [Show full text]
  • Sotos Syndrome
    European Journal of Human Genetics (2007) 15, 264–271 & 2007 Nature Publishing Group All rights reserved 1018-4813/07 $30.00 www.nature.com/ejhg PRACTICAL GENETICS In association with Sotos syndrome Sotos syndrome is an autosomal dominant condition characterised by a distinctive facial appearance, learning disability and overgrowth resulting in tall stature and macrocephaly. In 2002, Sotos syndrome was shown to be caused by mutations and deletions of NSD1, which encodes a histone methyltransferase implicated in chromatin regulation. More recently, the NSD1 mutational spectrum has been defined, the phenotype of Sotos syndrome clarified and diagnostic and management guidelines developed. Introduction In brief Sotos syndrome was first described in 1964 by Juan Sotos Sotos syndrome is characterised by a distinctive facial and the major diagnostic criteria of a distinctive facial appearance, learning disability and childhood over- appearance, childhood overgrowth and learning disability growth. were established in 1994 by Cole and Hughes.1,2 In 2002, Sotos syndrome is associated with cardiac anomalies, cloning of the breakpoints of a de novo t(5;8)(q35;q24.1) renal anomalies, seizures and/or scoliosis in B25% of translocation in a child with Sotos syndrome led to the cases and a broad variety of additional features occur discovery that Sotos syndrome is caused by haploinsuffi- less frequently. ciency of the Nuclear receptor Set Domain containing NSD1 abnormalities, such as truncating mutations, protein 1 gene, NSD1.3 Subsequently, extensive analyses of missense mutations in functional domains, partial overgrowth cases have shown that intragenic NSD1 muta- gene deletions and 5q35 microdeletions encompass- tions and 5q35 microdeletions encompassing NSD1 cause ing NSD1, are identifiable in the majority (490%) of 490% of Sotos syndrome cases.4–10 In addition, NSD1 Sotos syndrome cases.
    [Show full text]
  • Stress Fracture in Club Foot
    Case Report Stress fracture in club foot Jayakrishnan K Narayana Kurup1,*, Imthias V Kottamttavida2, Hitesh Shah3 1,2Senior Resident, 3Associate Professor, Dept. of Orthopaedics, Kasturba Medical College, Manipal University, Manipal, Karnataka *Corresponding Author: Email: [email protected] Abstract Stress fracture is rare in children. It is mostly described in adolescent involved in sports, athletics or dancing. Stress fracture in club foot is extremely rare; it might be due to the altered anatomy and may be a source of pain. We present a 6 year old girl with bilateral relapsed club feet with stress fracture of the proximal third of the fourth metatarsal on the left side. Correction of the deformity, cast immobilization and non-weight bearing led to the union of the fracture. Early correction of the deformity is justified to prevent recurrence of fractures. Key words: Stress fracture, Children, Club foot, Relapse, Deformity Key message: In children with relapsed or recurrent club foot, pain over the foot on walking and activity should be evaluated for possibility of a stress fracture. An early correction of the deformity is required to treat stress fractures. Access this article online were noted. The deformity progressed after the age of 2 Quick Response years. Bilateral deformity of hind foot varus and equinus, Code: Website: forefoot adduction and cavus were noted on clinical www.innovativepublication.com examination. Left side deformities were not passively correctable. There was callosity over the later border of both feet. There was no tenderness anywhere in the left DOI: foot. Her Body Mass Index (BMI) was 17 kg/m2 (normal 10.5958/2395-1362.2016.00025.6 for her age).
    [Show full text]
  • 23 Chromosome Trisomy 18 Syndrome
    638 Chromosome Trisomy 18 Syndrome 23 Chromosome Trisomy 18 Syndrome Edwards syndrome • Wide fontanels • Wormian bones Developmental and mental retardation, dolicho- • Thin calvaria cephaly, short palpebral fissures, micrognathia, over- • Hypoplasia of periorbital ridges lapping fingers, rocker-bottom feet • Hyper- or hypotelorism • Micrognathia (96%) Frequency: 1 in 5,000 births. Hands and Feet • Clenched hands, overlapping fingers Genetics • Ulnar deviation of the hand Trisomy 18; maternal age is a risk factor for aneu- • Hypoplastic thumbs, short 1st metacarpal ploidy; critical segment 18q11-q12. • Syndactyly, polydactyly, ectrodactyly • Short, hypoplastic, or absent finger phalanges Clinical Features • Equinovarus feet, rocker-bottom feet • Growth deficiency, failure to thrive • Toe syndactyly (2nd and 3rd toes most frequently • Hypoplastic skeletal muscle and subcutaneous fat involved) • Microcephaly, narrow bifrontal diameter, promi- • Hypoplastic, absent proximal hallucal phalanx nent occiput • Dysmorphic/absent toe phalanges • Short palpebral fissures, epicanthal folds, ptosis, Extremities microphthalmia, corneal opacities • Most pronounced changes involve the mesomelic • Short upper lip, small mouth, cleft lip/palate segments of the limbs • Micrognathia • Thin long bones • Low-set, dysplastic ‘fawn-like,’ posteriorly rotated • Tibial aplasia ears • Patellar aplasia • Shield-chest, short sternum, hypoplastic nipples • Genu valgum • Umbilical and inguinal hernia, diastasis recti • Radial hypoplasia • Cryptorchidism, hypoplastic labia
    [Show full text]
  • Phenotypes of a Family with XLH with a Novel PHEX Mutation Akiko Yamamoto 1, Toshiro Nakamura1,Yasuhisaohata 2, Takuo Kubota2 and Keiichi Ozono2
    Yamamoto et al. Human Genome Variation (2020) 7:8 https://doi.org/10.1038/s41439-020-0095-1 Human Genome Variation DATA REPORT Open Access Phenotypes of a family with XLH with a novel PHEX mutation Akiko Yamamoto 1, Toshiro Nakamura1,YasuhisaOhata 2, Takuo Kubota2 and Keiichi Ozono2 Abstract X-linked hypophosphatemia (XLH) is the most common form of heritable hypophosphatemic rickets. We encountered a 4-year-old boy with a novel variant in the phosphate-regulating neutral endopeptidase homolog X-linked (PHEX) gene who presented with a short stature, genu valgum, and scaphocephaly. The same mutation was identified in his mother and sister; however, the patient presented with a more severe case. X-linked hypophosphatemia (XLH) is an X-linked whereas his elder and younger brothers did not have a dominant disorder and the most common form of heri- short stature (Fig. 1(a)). table rickets, with a case rate estimate of ~1 case per At the time of his visit, his height was 95.4 cm 20,000 live births1. Inactive mutations in PHEX, which is (−2.51 standard deviation score (SDS)), weight was located in Xp22.1-22.2, have been implicated in the 14.8 kg (−1.13 SDS), and growth rate was 5.2 cm per year pathogenesis of XLH. More than 200 different mutations (−1.40 SDS), and genu valgum and scaphocephaly were in PHEX have been identified to date2. XLH is char- both evident. He did not have any dental issues or other acterized by rickets accompanied by bone deformities, a symptoms. fi 1234567890():,; 1234567890():,; 1234567890():,; 1234567890():,; short stature, dental anomalies, bone pain, hearing dif - His serum calcium level was 9.71 mg/dl (normal culties, enthesopathy, and muscular dysfunction3.
    [Show full text]
  • Expanded Indications for Guided Growth in Pediatric Extremities
    Current Concept Review Expanded Indications for Guided Growth in Pediatric Extremities Teresa Cappello, MD Shriners Hospitals for Children, Chicago, IL Abstract: Guided growth for coronal plane knee deformity has successfully historically been utilized for knee val- gus and knee varus. More recent use of this technique has expanded its indications to correct other lower and upper extremity deformities such as hallux valgus, hindfoot calcaneus, ankle valgus and equinus, rotational abnormalities of the lower extremity, knee flexion, coxa valga, and distal radius deformity. Guiding the growth of the extremity can be successful and is a low morbidity method for correcting deformity and should be considered early in the treatment of these conditions when the child has a minimum of 2 years of growth remaining. Further expansion of the application of this concept in the treatment of pediatric limb deformities should be considered. Key Concepts: • Guiding the growth of pediatric physes can successfully correct a variety of angular and potentially rotational deformities of the extremities. • Guided growth can be performed using a variety of techniques, from permanent partial epiphysiodesis to tem- porary methods utilizing staples, screws, or plate and screw constructs. • Utilizing the potential of growth in the pediatric population, guided growth principals have even been success- fully applied to correct deformities such as knee flexion contractures, hip dysplasia, femoral anteversion, ankle deformities, hallux valgus, and distal radius deformity. Introduction Guiding the growth of pediatric orthopaedic deformities other indications and uses for guided growth that may is represented by the symbol of orthopaedics itself, as not have wide appreciation. the growth of a tree is guided as it is tethered to a post (Figure 1).
    [Show full text]
  • Role of Talectomy in Severe Resistant Clubfoot in Children Mohammad a Hegazy1, Hossam M Khairy2, Sherif M El-Aidy3
    RESEARCH ARTICLE Role of Talectomy in Severe Resistant Clubfoot in Children Mohammad A Hegazy1, Hossam M Khairy2, Sherif M El-Aidy3 ABSTRACT Despite of the global attention paid to talectomy in management of severe, rigid, and resistant deformities of clubfoot, no evaluation of this procedure has been done before in our institution. The aim of work was to evaluate the outcome of surgical removal of talus in these patients. Seventeen severe, rigid, and resistant clubfeet in 10 patients undergoing talectomy were evaluated pre- and postoperative at the Department of Orthopedic Surgery, Zagazig University hospitals, Al-Sharkia, Egypt. The collected data were statistically analyzed. Out of the 10 investigated cases, there were seven males and three females. Seven (70%) cases were bilaterally affected; only three (30%) were one-sided affected. They were one left-sided in two cases and the other was right-sided. Their age ranged 1–5 years with a mean of 30.2 ± 13.3 months. There were good results in 11 (65%) cases out of the 17 operated. Fair results were found in 6 (35%) cases. Three from the 6 feet with fair results following talectomy showed residual cavus; and the others were noticed with residual hindfoot varus with slight inversion and adduction of the forefoot. All cases were with stable and plantigrade foot. In general, patients of both good and fair results were being able to wear shoes and to walk independently with pain free movements. Talectomy could be considered as a single salvage procedure for cases of clubfoot suffering from rigid, resistant and severe deformities.
    [Show full text]
  • 14 Carpenter Syndrome
    614 Carpenter Syndrome 14 Carpenter Syndrome Acro-cephalo-polysyndactyly Type II, ACPS II Hands • Brachydactyly, stubby fingers Acrocephaly, peculiar facies, syndactyly of fingers, • Short or absent middle phalanges polysyndactyly of toes, obesity, mental retardation • Soft tissue syndactyly (mostly involving 3rd and 4th fingers) Frequency: Rare. • Clinodactyly • Camptodactyly Genetics • Duplication of the proximal phalanx of the thumbs Autosomal recessive (OMIM 201000); Goodman Feet syndrome (OMIM 201220) and Summitt syndrome • Preaxial polydactyly (OMIM 272350) are within the clinical spectrum of • Partial syndactyly ACPS II. • Short or absent middle phalanges • Metatarsus varus Clinical Features Extremities • Acrocephaly, asymmetrical turricephaly, promi- • Genu valgum nent metopic ridge • Laterally displaced patella • Flat facies, shallow orbits, hypertelorism, epican- Pelvis thal folds, lateral displacement of medial canthi, • Flared ilia downward palpebral fissures, broad cheeks, nar- • Poorly developed acetabula row maxilla, high palate, low set ears • Coxa valga • Small genitalia • Genu valgum, lateral position of the patella • Finger brachydactyly, syndactyly Bibliography • Pes varus, broad hallux, preaxial polydactyly of toes Cohen DM, Green JG, Miller J, Gorlin RJ, Reed JA. Acro- • Congenital heart disease cephalopolysyndactyly type II-Carpenter syndrome: clini- • cal spectrum and an attempt at unification with Goodman Truncal obesity in older patients and Summitt syndromes.Am J Med Genet 1987; 28: 311–24 • Variable mental retardation Gershoni-Baruch R. Carpenter syndrome: marked variability of expression to include the Summitt and Goodman syn- Differential Diagnosis dromes. Am J Med Genet 1990; 35: 236–40 • Goodman syndrome Richieri-Costa A,Pirolo Junior L,Cohen MM Jr.Carpenter syn- • drome with normal intelligence: Brazilian girl born to con- Summit syndrome sanguineous parents.
    [Show full text]