The Causes of Congenital Club Foot
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Tracheal Perforation in a Neonate: a Devastating
Letters to Editor Tracheal perforation in a size of endotracheal tube, cuff overinflation, cough and vigorous movements of head and neck.[2,3] neonate: A devastating Neonatal tracheal injury is ascribed to factors like complication following traumatic traumatic delivery, weak trachea, congenital tracheal endotracheal intubation stenosis, ring agenesis, metal stylets, rigid endotracheal tube, excessive external laryngeal pressure and [1,4,5] Sir, prolonged ventilation. Tracheal injury in neonates following endotracheal In our case, rigorous attempts at intubation along with intubation represents an uncommon complication excessive hyperextension of head and neck due to altered rarely described in literature but carries high anatomy are likely to have contributed to tracheal injury. morbidity and a mortality rate of 70%.[1] We describe Multiple attempts at intubation are known to result in a [4] a case of neonatal tracheal perforation following false tract and are related to anterior tracheal lesions. multiple attempts at endotracheal intubation due to an Incidentally, our case was an undiagnosed Pierre unanticipated difficulty in an emergency situation in Robins Sequence. A small receding mandible, tongue an undiagnosed case of Pierre Robin Sequence. immobility and cleft palate are identified as independent factors for difficult airway with a risk of upper airway A 4-week-old female baby presented to the emergency obstruction, difficult mask holding, difficult intubation, department with respiratory difficulty. In view of severe leak through the cleft resulting in inadequate ventilation respiratory distress and desaturation (SpO2- 60%) a as well as passage of the endotracheal tube into the decision was made to provide ventilatory support to cleft.[6] Successful airway management in such situation the neonate. -
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). -
Spinal Deformity Study Group
Spinal Deformity Study Group Editors in Chief Radiographic Michael F. O’Brien, MD Timothy R. Kuklo, MD Kathy M. Blanke, RN Measurement Lawrence G. Lenke, MD Manual B T2 T5 T2–T12 CSVL T5–T12 +X° -X +X° C7PL T12 L2 A S1 ©2008 Medtronic Sofamor Danek USA, Inc. – 0 + Radiographic Measurement Manual Editors in Chief Michael F. O’Brien, MD Timothy R. Kuklo, MD Kathy M. Blanke, RN Lawrence G. Lenke, MD Section Editors Keith H. Bridwell, MD Kathy M. Blanke, RN Christopher L. Hamill, MD William C. Horton, MD Timothy R. Kuklo, MD Hubert B. Labelle, MD Lawrence G. Lenke, MD Michael F. O’Brien, MD David W. Polly Jr, MD B. Stephens Richards III, MD Pierre Roussouly, MD James O. Sanders, MD ©2008 Medtronic Sofamor Danek USA, Inc. Acknowledgements Radiographic Measurement Manual The radiographic measurement manual has been developed to present standardized techniques for radiographic measurement. In addition, this manual will serve as a complimentary guide for the Spinal Deformity Study Group’s radiographic measurement software. Special thanks to the following members of the Spinal Deformity Study Group in the development of this manual. Sigurd Berven, MD Hubert B. Labelle, MD Randal Betz, MD Lawrence G. Lenke, MD Fabien D. Bitan, MD Thomas G. Lowe, MD John T. Braun, MD John P. Lubicky, MD Keith H. Bridwell, MD Steven M. Mardjetko, MD Courtney W. Brown, MD Richard E. McCarthy, MD Daniel H. Chopin, MD Andrew A. Merola, MD Edgar G. Dawson, MD Michael Neuwirth, MD Christopher DeWald, MD Peter O. Newton, MD Mohammad Diab, MD Michael F. -
Podo Pediatrics Podo Pediatrics
Podo Pediatrics Identifying Biomechanical Pathologies David Lee, D.P.M., D. A.B.P.S. Purpose • Identification of mechanical foot and ankle conditions • Base treatments • Knowing when to refer to a podiatrist Topics • Flatfoot (Pes Plano Valgus) • Equinus • Intoed feet (Cavo-adductor Varus) • Heel pain (Calcaneodynia) • Shin Splints • Various Pedal deformities 1 WHAT IS NORMAL? At birth to ~9 months • Ankle flexible to over 20 deg DF • No “C” shaped foot • No clicking or popping sounds • Babinski sign • Pull up 7-8mo. 9-16 months… • Begin walking • Feet are fat, flat and floppy • Knees are always center or externally rotated, never internal. • Stance is wide and less stable • Stomping gait pattern 2 16-18 months • Able to walk upstairs • Knee never internal • Still wide base and flat and floppy feet • Stomping still 3-7 years • Able toe walk downstairs • Heel-to-toe walk • Watch for – Intoeing – Tripping – Tight ankle joint (equinus) 7 years and up • Arch should be developed • Heel-to-toe walk • Heel is perpendicular to ground • Knees straight ahead 3 Neutral Internal Rotation Early detection is important • Prevent long term adaptation • Joint damage • Adult pathology – Heel pain, bunions, hammertoes, ankle instability, knee pain, shin splints, etc. • Ability to thrive physically and socially 4 THE FLAT FOOT Visual Complaints by the Parent • Tripping or falling • Poor balance- Clumsy • Feet look funny, walks funny • Shoes wearing out quickly Social Complaints by the Parent • Lazy, inactive, “doesn’t like going outside to play or play sports -
Hallux Valgus
MedicalContinuing Education Building Your FOOTWEAR PRACTICE Objectives 1) To be able to identify and evaluate the hallux abductovalgus deformity and associated pedal conditions 2) To know the current theory of etiology and pathomechanics of hallux valgus. 3) To know the results of recent Hallux Valgus empirical studies of the manage- ment of hallux valgus. Assessment and 4) To be aware of the role of conservative management, faulty footwear in the develop- ment of hallux valgus deformity. and the role of faulty footwear. 5) To know the pedorthic man- agement of hallux valgus and to be cognizant of the 10 rules for proper shoe fit. 6) To be familiar with all aspects of non-surgical management of hallux valgus and associated de- formities. Welcome to Podiatry Management’s CME Instructional program. Our journal has been approved as a sponsor of Continu- ing Medical Education by the Council on Podiatric Medical Education. You may enroll: 1) on a per issue basis (at $15 per topic) or 2) per year, for the special introductory rate of $99 (you save $51). You may submit the answer sheet, along with the other information requested, via mail, fax, or phone. In the near future, you may be able to submit via the Internet. If you correctly answer seventy (70%) of the questions correctly, you will receive a certificate attesting to your earned credits. You will also receive a record of any incorrectly answered questions. If you score less than 70%, you can retake the test at no additional cost. A list of states currently honoring CPME approved credits is listed on pg. -
Orthopedic-Conditions-Treated.Pdf
Orthopedic and Orthopedic Surgery Conditions Treated Accessory navicular bone Achondroplasia ACL injury Acromioclavicular (AC) joint Acromioclavicular (AC) joint Adamantinoma arthritis sprain Aneurysmal bone cyst Angiosarcoma Ankle arthritis Apophysitis Arthrogryposis Aseptic necrosis Askin tumor Avascular necrosis Benign bone tumor Biceps tear Biceps tendinitis Blount’s disease Bone cancer Bone metastasis Bowlegged deformity Brachial plexus injury Brittle bone disease Broken ankle/broken foot Broken arm Broken collarbone Broken leg Broken wrist/broken hand Bunions Carpal tunnel syndrome Cavovarus foot deformity Cavus foot Cerebral palsy Cervical myelopathy Cervical radiculopathy Charcot-Marie-Tooth disease Chondrosarcoma Chordoma Chronic regional multifocal osteomyelitis Clubfoot Congenital hand deformities Congenital myasthenic syndromes Congenital pseudoarthrosis Contractures Desmoid tumors Discoid meniscus Dislocated elbow Dislocated shoulder Dislocation Dislocation – hip Dislocation – knee Dupuytren's contracture Early-onset scoliosis Ehlers-Danlos syndrome Elbow fracture Elbow impingement Elbow instability Elbow loose body Eosinophilic granuloma Epiphyseal dysplasia Ewing sarcoma Extra finger/toes Failed total hip replacement Failed total knee replacement Femoral nonunion Fibrosarcoma Fibrous dysplasia Fibular hemimelia Flatfeet Foot deformities Foot injuries Ganglion cyst Genu valgum Genu varum Giant cell tumor Golfer's elbow Gorham’s disease Growth plate arrest Growth plate fractures Hammertoe and mallet toe Heel cord contracture -
Supplemental Information
REVIEW ARTICLE Supplemental Information SEARCH STRATEGIES 7. exp Congenital Abnormalities/ or remifentanil or sufentanil or 8. (defect or cleft or heart defect tapentadol or tramadol or heroin Database: Ovid MEDLINE(R) In- or nalmefene or naloxone or Process and Other Nonindexed or gastroschisis or cryptorchidism or atresia or congenital or clubfoot naltrexone).mp. Citations and Ovid MEDLINE(R), or renal or craniosynostosis or 4. 1 or 2 or 3 1946 to Present hypospadias or malformation or 5. exp pregnancy/or exp pregnancy spina bifida or neural tube defect). outcome/ mp. 1. exp Analgesics, Opioid/ 6. exp teratogenic agent/ 9. 5 or 6 or 7 or 8 2. (opioid* or opiate*).mp. 7. exp congenital disorder/ 10. 4 and 9 3. (alfentanil or alphaprodine or 11. Limit 10 to (English language and 8. (defect or cleft or heart defect buprenorphine or butorphanol humans) or gastroschisis or cryptorchidism or codeine or dezocine or or atresia or congenital or clubfoot dihydrocodeine or fentanyl or Database: Ovid Embase, 1988– or renal or craniosynostosis or hydrocodone or hydromorphone 2016, Week 7 hypospadias or malformation or or levomethadyl or levorphanol spina bifida or neural tube defect). or meperidine or methadone or mp. 1. exp opiate/ morphine or nalbuphine or opium 9. 5 or 6 or 7 or 8 or oxycodone or oxymorphone 2. (opioid* or opiate*).mp. or pentazocine or propoxyphene 10. 4 and 9 3. (alfentanil or alphaprodine or or remifentanil or sufentanil or buprenorphine or butorphanol 11. Limit 10 to (human and English tapentadol or tramadol or heroin or codeine or dezocine or language and (article or book or or nalmefene or naloxone or book series or conference paper dihydrocodeine or fentanyl or “ ” naltrexone).mp. -
Saethre-Chotzen Syndrome
Saethre-Chotzen syndrome Authors: Professor L. Clauser1 and Doctor M. Galié Creation Date: June 2002 Update: July 2004 Scientific Editor: Professor Raoul CM. Hennekam 1Department of craniomaxillofacial surgery, St. Anna Hospital and University, Corso Giovecca, 203, 44100 Ferrara, Italy. [email protected] Abstract Keywords Disease name and synonyms Excluded diseases Definition Prevalence Management including treatment Etiology Diagnostic methods Genetic counseling Antenatal diagnosis Unresolved questions References Abstract Saethre-Chotzen Syndrome (SCS) is an inherited craniosynostotic condition, with both premature fusion of cranial sutures (craniostenosis) and limb abnormalities. The most common clinical features, present in more than a third of patients, consist of coronal synostosis, brachycephaly, low frontal hairline, facial asymmetry, hypertelorism, broad halluces, and clinodactyly. The estimated birth incidence is 1/25,000 to 1/50,000 but because the phenotype can be very mild, the entity is likely to be underdiagnosed. SCS is inherited as an autosomal dominant trait with a high penetrance and variable expression. The TWIST gene located at chromosome 7p21-p22, is responsible for SCS and encodes a transcription factor regulating head mesenchyme cell development during cranial tube formation. Some patients with an overlapping SCS phenotype have mutations in the FGFR3 (fibroblast growth factor receptor 3) gene; especially the Pro250Arg mutation in FGFR3 (Muenke syndrome) can resemble SCS to a great extent. Significant intrafamilial -
Loss of Correction in Cubitus Varus Deformity After Osteotomy
Loss of correction in cubitus varus deformity after osteotomy Chao You Shenzhen children's hospital Yibiao Zhou Shenzhen children's hospital https://orcid.org/0000-0001-9754-1089 Jingming Han ( [email protected] ) Research article Keywords: cubitus varus osteotomy Loss of correction Posted Date: May 5th, 2020 DOI: https://doi.org/10.21203/rs.3.rs-26279/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/14 Abstract Purpose Cubitus varus deformity in the pediatric population is an infrequent but clinically important disease to orthopedic surgeons. Since these patient populations are different in many respects, we sought out to investigate the rates of loss of correction over time as well as the factors associated with loss of correction in pediatric patients undergoing osteotomy for treatment of cubitus varus deformity. Methods Between 2008-7 and 2017-7, we treated 30 cases of cubital varus had underwent the the osteotomy. We compared preoperative and postoperative clinical and imaging parameters (H-cobb angle,Baumman angle) for all patients. Postoperative evaluation was performed by telephone interview. Results In our study,there were 30 patients,included 17 males and 13 females.the mean age was 75 months old.In the rst follow-up,Approximately 80 % of patients had a loss of correction of H-cobband 83% of patients at the second follow-up. The Baumann angle also had a loss of correction,about 57% was lost at the rst follow-up,and 43% was lost at the second follow-up. The average interval between the rst follow-up and the second follow-up was 24 days The H-cobb angle mean loss was 2.4°.There was a statistically signicant difference between the H-cobb angle measured before surgery and the angle measured after surgery (p <0.05). -
Angular Limb Deformities in Foals: Treatment and Prognosis*
Article #4 CE Angular Limb Deformities in Foals: Treatment and Prognosis* Nicolai Jansson, DVM, PhD, DECVS Skara Equine Hospital Skara, Sweden Norm G. Ducharme, DVM, MSc, DACVS Cornell University ABSTRACT: This article presents an overview of the clinical management of foals with angular limb deformities. Both conservative and surgical treatment options exist; the choice of which to use should be based on the type, severity, and location of the deformity as well as the age of the foal. Conservative measures include controlled exercise, rigid external limb support, and corrective hoof trimming. Surgical treatment modalities comprise tech- niques for manipulating physeal growth and, after physeal closure, various corrective osteotomy or ostectomy methods. The prognosis is generally good if treatment is initi- ated well in advance of physeal closure. ngular limb deformities and their treat- Conservative Treatment ment in foals and young horses constitute In most foals born with mild to moderate a significant part of the orthopedic prob- angular deformities, spontaneous resolution A 2 lems that veterinarians must manage. This article occurs within the first 2 to 4 weeks of life. In discusses the clinical management and prognosis newborn foals, periarticular laxity is the most of these postural deformities. likely cause, and these foals require no special treatment other than a short period of con- TREATMENT trolled exercise. In our opinion, mildly and The absence of controlled studies has moderately affected foals should not be confined impaired the accumulation of scientific data to a stall because exercise is important for nor- guiding the management of angular limb defor- mal muscular development and resolution of the mities in foals (Table 1). -
Spinal Dysraphism an Orthopaedic Syndrome in Children Accompanying Occult Forms
Arch Dis Child: first published as 10.1136/adc.35.182.315 on 1 August 1960. Downloaded from SPINAL DYSRAPHISM AN ORTHOPAEDIC SYNDROME IN CHILDREN ACCOMPANYING OCCULT FORMS BY C. C. MICHAEL JAMES and L. P. LASSMAN From the Departments of Orthopaedic Surgery and Neurological Surgery, Newcastle General Hospital, Newcastle upon Tyne (RECEIVED FOR PUBLICATION OCTOBER 19, 1959) Much interest has been shown in the pathology which usually suffer. The treatment in the first of the more gross developmental anomalies of the place is principally in the field of neurosurgery since spinal cord and its coverings and in their clinical the removal of the primary cause, when it is possible, manifestations, most of which are not amenable to demands laminectomy and exploration around the treatment. It has not been appreciated that lesser spinal cord within the dura mater. Subsequent anomalies can also produce disabilities, that they orthopaedic care will be needed only to correct can be diagnosed in life and that they can frequently established deformity if the diagnosis has been be treated by surgery before the secondary effects made late. have become severe and irreversible. Clinical Spinal dysraphism is a term which has been experience over a number of years of the many applied to failure of complete development in the copyright. children sent to orthopaedic clinics with various midline of the dorsal aspect of the embryo. The types of foot or lower limb defect led us to suspect extent of this failure may be of mild, moderate or the presence in some children of a spinal cord severe degree. -
Crouzon Syndrome with Ophthalmological Complications
Journal of Rawalpindi Medical College (JRMC); 2012;16(1):80-81 Case Report Crouzon Syndrome With Ophthalmological Complications Rahela Nasir Paediatric Department, Capital Hospital, CDA Islamabad. Crouzon Syndrome is characterized by premature bilateral optic atrophy. Other facial features included a craniosynostosis. It has an autosomal dominant inheritance prominent nose and deep and narrow palate. No but represents fresh mutation also. Other craniofacial digital abnormalities were seen. No dental aplasia was abnormalities include ocular proptosis caused by shallow present. Systemic examination revealed no orbits with or without divergent strabismus. There may be abnormality. increased intracranial pressure for which surgical morcellation procedures are indicated. A case of He was diagnosed as a case of Crouzon syndrome craniosynostosis is reported which is diagnosed as Crouzon with ocular complications on clinical basis. He was Syndrome with ocular complications on clinical grounds. investigated for microcephaly and suspected Split craniotomy was performed by a neurosurgeon to craniosynostosis. Radiographs of skull showed small relieve raised intracranial pressure and to enhance brain sized skull with early closure of sutures and fontanelle growth. Crouzon Syndrome was originally described in 1912 suggestive of craniosynstosis(Fig 2). A hammered- by Crouzon in a mother and her daughter. It is an autosomal silver (beaten metal/ copper beaten) appearance was dominant inherited disorder but represents fresh mutation also seen due to raised intracranial pressure and also. Crouzon syndrome is characterized by premature compression of the developing brain on the fused craniosynostosis which is quite variable but the coronal suture is nearly always bilaterally involved. Craniofacial bone. CT scan brain with contrast was done which abnormalities include brachycephaly, shallow orbits and confirmed the features suggestive of craniosynostosis maxillary hypoplasia.