Pathogenetic mechanisms of fetal akinesia deformation sequence and oligohydramnios sequence
Corresponding Author
Dr. José Ignacio Rodríguez
Department of Pathology, Hospital La Paz, Madrid, Spain
Departamento de Anatomía Patológica, Hospital La Paz, Paseo de la Castellana 261, E-28046 Madrid, SpainSearch for more papers by this authorJosé Palacios
Department of Pathology, Hospital La Paz, Madrid, Spain
Search for more papers by this authorCorresponding Author
Dr. José Ignacio Rodríguez
Department of Pathology, Hospital La Paz, Madrid, Spain
Departamento de Anatomía Patológica, Hospital La Paz, Paseo de la Castellana 261, E-28046 Madrid, SpainSearch for more papers by this authorJosé Palacios
Department of Pathology, Hospital La Paz, Madrid, Spain
Search for more papers by this authorAbstract
This article briefly reviews the participation of fetal compression, muscular weakness, and fetal akinesia in the genesis of the anomalies found in fetal akinesia deformation sequence (FADS) and oligohydramnios sequence (OS). Both sequences share phenotypic manifestations, such as arthrogryposis, short umbilical cord, and lung hypoplasia, in relation to decreased intrauterine fetal motility. Other characteristic manifestations found in OS, such as Potter face, and redundant skin, are produced by fetal compression. On the other hand, growth retardation, craniofacial anomalies, micrognathia, long bone hypoplasia, and polyhydramnios found in FADS could be related to intrauterine muscular weakness.
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