• P Marcorelles.
• Service d'anatomie pathologique, pôle biologie pathologie, hôpital Morvan, CHRU, 5 avenue Foch, 29609 Brest cedex, France. Electronic address: pascale.marcorelles@chu-brest.fr.
• J Gynecol Obstet Biol Reprod (Paris). 2013 Dec 1; 42 (8): 996-1007.

ObjectiveTo evaluate the placental pathological patterns in intrauterine growth restriction (IUGR) in order to determinate which placental lesions are linked to clinically significant anomalies and to predict the child outcome and the mother risk of recurrence.MethodsBibliographic review using the Medline and PubMed databases.ResultsPlacental studies designed in order to provide macroscopic and microscopic information about the mechanism of IUGR are not numerous and retrospective; files are most of the time very small. Meta-analyses are an exception. Maternal vascular underperfusion is admitted to be the most frequent etiology of IUGR. None of the associated placental lesions is pathognomonic but the combination of a number of placental changes is. Low placental weight and microscopic lesions are more frequent than gross anomalies. Other pathophysiological groups of placental pathologies are reported to be linked to fetal growth restriction: umbilical cord anomalies, fetal thrombotic vasculopathy, chronic villitis of unknown etiology and chronic histiocytic intervillositis. Some placental lesions have been reported associated with infants with neurologic impairment and can be as different as vascular lesions, villitis of unknown origin with stem villi vasculopathy, fetal thrombotic vasculopathy or umbilical cord anomalies. However, there is no direct link between a type of placental pathology and the infant's adverse outcome or his neurological risk. The maternal risk of recurrence is not easily predictable except for the chronic histiocytic intervillositis in which the estimated recurrence rate is very high.ConclusionPlacental morphological findings can play a critical role in explaining the IUGR. They always need to be correlated with clinical findings.Copyright © 2013. Published by Elsevier Masson SAS.

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