The placenta in preterm birth

Abstract

Rates of preterm birth range from 5% to 13% of deliveries in developed countries. About two-thirds of preterm deliveries are due to spontaneous onset of preterm labour or preterm premature rupture of membranes. Approximately one-third follow induction of labour or caesarean section performed for maternal or fetal indications such as preeclampsia, haemorrhage, non-reassuring fetal heart rate or intrauterine growth restriction. Thus, pathologists are frequently called on to evaluate preterm placentas, to determine the cause of the spontaneous preterm birth and/or correlate placental findings with the clinical history. This review provides pathologists with an overview of the recent clinical research in the pathogenesis of preterm birth and relates these to the correlative placental pathologies of the major causes of spontaneous preterm birth. A brief summary of the placental gross and histopathological findings in indicated preterm birth is also included.

Does aetiology of neonatal encephalopathy and hypoxic–ischaemic encephalopathy influence the outcome of treatment?

“…23 The prevalence of chronic villitis increases with gestational age, and is associated with a marked increase in the risk of neonatal encephalopathy. 24,25 Chronic villitis may coexist with, or be difficult to distinguish from, fetal thrombotic vasculopathy of the placenta, 26 which is also associated with the risk of adverse neurological outcomes, 24,25 and with stillbirth and cardiac malformations. 26 Risk factors for both chronic villitis and adverse neurological outcomes include prior pregnancy loss, fetal growth restriction, abnormal fetal heart rate patterns, need for emergency surgical delivery, severe acidosis, and neuroimaging evidence of basal ganglia-thalamic injury.…”

“…24,25 Chronic villitis may coexist with, or be difficult to distinguish from, fetal thrombotic vasculopathy of the placenta, 26 which is also associated with the risk of adverse neurological outcomes, 24,25 and with stillbirth and cardiac malformations. 26 Risk factors for both chronic villitis and adverse neurological outcomes include prior pregnancy loss, fetal growth restriction, abnormal fetal heart rate patterns, need for emergency surgical delivery, severe acidosis, and neuroimaging evidence of basal ganglia-thalamic injury. 27 Some of these characteristics are sometimes assumed to be indicators of birth asphyxia but, since they are not specific to birth asphyxia, the possibility of misattribution of aetiology is high without a placental histological examination carried out by an experienced perinatal pathologist.…”

Chorioamnionitis: a multiorgan disease of the fetus?

“…These may be diagnosed by culture or proteomic profiling of the amniotic fluid, by microbial culture or footprinting, or by histological examination of the placenta after birth. 5 The latter is generally regarded as the 'gold standard' in the diagnosis of chorioamnionitis. 5 More serious cases of chorioamnionitis may become clinically apparent and cause both general (fever, leukocytosis and raised C-reactive protein) and local symptoms (uterine tenderness and vaginal discharge).…”

“…5 The latter is generally regarded as the 'gold standard' in the diagnosis of chorioamnionitis. 5 More serious cases of chorioamnionitis may become clinically apparent and cause both general (fever, leukocytosis and raised C-reactive protein) and local symptoms (uterine tenderness and vaginal discharge). Although a combination of these symptoms is often given the syndromic description 'clinical chorioamnionitis', the overlap with the histological diagnosis of chorioamnionitis has been shown to be only modest.…”

“…and Mycoplasma spp. 2,5 Both the maternal and fetal immune system have an important role in chorioamnionitis, given the shown associations between polymorphisms in immunoregulatory genes and the risk of chorioamnionitis and preterm labor. 6,7 A large subset of chorioamnionitis cases remain clinically silent.…”