Traditional methods of correcting malunited distal humeral fractures in children involve complex wedge osteotomies held with pins or internal fixation devices. These require a large exposure and challenging fixation. We elected to perform simple transverse osteotomies, without wedges, using a lateral incision. These were maintained by the small AO external fixator. Between 1987 and 2004, five children with malunited distal humeral fractures were treated. Angular and rotational correction was obtained in each case. Bony union occurred at an average of 8 weeks. A simple osteotomy held by the small AO external fixator provides accurate correction, precise adjustability, and solid stability.
SUMMARY In order to test the possibility that neuromuscular abnormality is the fundamental cause of congenital club foot, a total of 90 muscle biopsies were taken from 13 patients with club feet requiring surgical correction. All the biopsies were studied electron microscopically, and abnormalities were seen in all instances. 48 of the biopsies (taken from nine of the 13 patients) were examined histochemically, and 42 of these showed an abnormally high proportion of slow twitch, high tension fibers (Type I), together with a proportionate increase in Type I neuromuscular junctions. These results suggest that there is a primary neuromuscular abnormality in rigid club‐foot: a subtle muscle imbalance present in early fetal life cause the deformity and induce the well‐recognized secondary abnormalities. RÉSUMÉ Pied bot: trouble neuromusculaire Pour vérifier si une anomalie neuromusculaire n'etait pas la cause fondamentale du pied bot congénital, un total de 90 biopsies musculaires ont été practiquées chez 13 sujets porteurs de pied bot exigeant une correction chirurgicale. Toutes les biopsies ont été examinées au microscope électronique et des anomalies ont été observées dans tous les cas. 48 des biopsies (prises chez neuf des 13 sujets) ont été examinées histochimiquement et 42 d'entre elles ont montré une proportion anormalement élevée de fibres lentes à forte tension (Type I), ainsi qu'une proportion accrue de jonctions neuromusculaires de Type I. Ces résultats suggèrent qu'il y a une anomalie neuromusculaire primaire dans le pied bot fixé: le déséquilibre musculaire cause la déformation et induit les anomalies secondaires bien connues. ZUSAMMENFASSUNG Klumpfufß: eine neuromuskuläre Erkrankung Zur Uberprüfung der Hypothese, daß neuromuskuläre Anomalien die eigentliche Ursache des kongenitalen Klumpfusses sind, wurden von Patienten, die operiert werden mußten, insgesamt 90 Muskelbiopsien entnommen. Alle Biopsien wurden elektronenmikroskopisch untersucht und bei allen wurden abnorme Befunde festgestellt. 48 der Biopsien (von neun der 13 Patienten) wurden histochemisch untersucht und 42 davon zeigten einen abnorm hohen Anteil von langsamen tonischen Fasern (Typ I) und einen entsprechend hohen Anteil neuromuskulärer Endplatten. Diese Ergebnisse weisen darauf hin, daß es eine primäre neuromuskuläre Anomalie beim rigiden Klumpfuß gibt: Störungen im Muskel verursachen die Mißbildung und führen die bekannten sekundären Anomalien herbei. RESUMEN Pié zambo: una enfermedad neuromuscular Con el objeto de dilucidar la posibilidad de que una anomalia neuromuscular sea la causa fundamental del pié zambo congénito, se realizaron 90 biopsias musculares en 13 pacientes con pié zambo que requeria correccion quirúrgica. Todas las biopsias fueron estudiadas con microscopia electrónica y en todos los casos se observaron anomalias. 48 de las biopsias (tomadas de neuve de los 13 pacientes) fueron examinadas histoquimicamente, y 42 ellas mostraban una proporción anormalmente alta de fibras de alta tensión y baja contracción (Tipo I), junto...
A 9-year-old girl with multiple osteochondromatosis presented with a 1 year history of a gradually enlarging surface lesion originating from the midsection of the right humerus, distal to an osteochondroma. Radiographically and histologically this lesion proved to be a periosteal chondrosarcoma adjacent to an osteochondroma.
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