RESUMEN
The accidental loss of fingertip soft tissues, which may expose tendons and bones, is a common injury in emergency departments. If these lesions are poorly treated, they can impair fine motor skills and tactile sensitivity of the fingertips. The study was conducted on 30 patients (24 males and 6 females) with 32 soft tissue defects of the fingertip treated in emergency plastic surgery with local pedicled flap at the Plastic Surgery Department of Saint Paul Hospital Hanoi from 01/2016 to 06/2017. The most common cause of injury (21/30) was occupational accidents. At the time of the accident, 12 patients did not have personal protective equipment (PPE). Among 18 patients who had one, eight had incomplete equipment. Of 32 implanted skin flaps, 31 survived completely without necrosis or infection, only one being affected by epidermolysis. Postoperative evaluation showed excellent motor skills for 31/32 fingers and a sensitivity restoration at S4 level for 27/32. Workplace accident is the main cause of fingers soft tissue defects. Covering the fingers soft tissue defects with local pedicled flap in emergency preserves the fine motor function and the delicated tactile sensation of the fingers.
Une étude sur les pertes de substance accidentelles de la pulpe des doigts et leur recouvrement par lambeaux locaux a été réalisée dans le service de chirurgie reconstructive de l'hôpital Saint Paul de Hanoï de janvier 2016 à juin 2017. Elle a concerné 30 patients, 24 hommes et 6 femmes. La cause la plus fréquente était l'accident de travail, soit 21/30 cas. Au moment de l'accident, 12 patients ne disposaient pas d'équipement de protection individuelle (EPI). Sur les 18 patients qui en possédaient, 8 avaient un équipement incomplet. Sur 32 lambeaux mis en place, 31 ont survécu complètement sans nécrose, ni infection, et un a subi une épidermolyse. Trente et un des 32 doigts opérés ont conservé une fonction motrice de bonne qualité et 27 ont récupéré une sensibilité de niveau S4. Le traitement en urgence des pertes de substance de la pulpe des doigts par des lambeaux locaux permet de préserver la fonction motrice fine et la sensibilité des pulpes des doigts.
Asunto(s)
Traumatismos de los Dedos/cirugía , Traumatismos Ocupacionales/cirugía , Procedimientos de Cirugía Plástica , Trasplante de Piel , Colgajos Quirúrgicos/trasplante , Accidentes de Trabajo/estadística & datos numéricos , Adolescente , Adulto , Anciano , Niño , Preescolar , Femenino , Traumatismos de los Dedos/epidemiología , Traumatismos de los Dedos/rehabilitación , Dedos/patología , Humanos , Estudios Longitudinales , Masculino , Persona de Mediana Edad , Traumatismos Ocupacionales/epidemiología , Traumatismos Ocupacionales/rehabilitación , Procedimientos de Cirugía Plástica/métodos , Procedimientos de Cirugía Plástica/rehabilitación , Procedimientos de Cirugía Plástica/estadística & datos numéricos , Recuperación de la Función/fisiología , Estudios Retrospectivos , Trasplante de Piel/métodos , Trasplante de Piel/rehabilitación , Trasplante de Piel/estadística & datos numéricos , Traumatismos de los Tejidos Blandos/epidemiología , Traumatismos de los Tejidos Blandos/rehabilitación , Traumatismos de los Tejidos Blandos/cirugía , Tacto/fisiología , Resultado del Tratamiento , Vietnam/epidemiología , Adulto JovenRESUMEN
Measles virus (MV) can infect mouse macrophages to cause a prolonged non-cytopathic infection that produces low levels of infectious virus for days. We have generated RAW264.7 mouse macrophages expressing human CD46, a cell surface complement regulatory protein that serves as a receptor for laboratory-adapted strains of MV. Laboratory-adapted MV strains efficiently enter the CD46-positive mouse macrophages to cause a cytopathic infection with extensive multinucleated cells and pseudopodia-like extensions. However, MV infection of mouse macrophages through CD46 is self-limiting. Both viral protein synthesis and infectious virus production are abruptly terminated after the second day of infection. This novel virus-cell interaction is seen only in mouse macrophages but not in mouse or hamster fibroblasts expressing human CD46. The possible role of CD46 in macrophage antiviral response restricting MV replication is discussed.
