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The Scottish Perinatal Neuropathology Study—clinicopathological correlation in stillbirths
Author(s) -
Becher JC,
Bell JE,
Keeling JW,
Liston WA,
McIntosh N,
Wyatt B
Publication year - 2006
Publication title -
bjog: an international journal of obstetrics and gynaecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.157
H-Index - 164
eISSN - 1471-0528
pISSN - 1470-0328
DOI - 10.1111/j.1471-0528.2006.00852.x
Subject(s) - neuropathology , medicine , fetus , obstetrics , pregnancy , population , gestation , brain damage , pathology , disease , biology , environmental health , genetics
Objective To examine the neuropathology of fetuses dying before birth, to determine the timing of any brain damage seen and to ascertain clinical associations of pre‐existing brain damage. Design Population‐based observational study. Setting All 22 delivery units within Scotland, 1995–1998. Sample All stillborn fetuses ≥24 weeks of gestation excluding those with chromosomal abnormality or central nervous system/cardiothoracic malformation. Methods Clinical detail was collected on all stillborn fetuses. Requests for postmortem included separate request for detailed neuropathological examination. Stillborn fetuses were classified as full term antepartum (normal growth/growth restricted), preterm antepartum (normal growth/growth restricted), intrapartum (full term/preterm), multiple births and stillborn fetuses following abruptions. Clinicopathological correlation attempted to define the timing of brain insult. Placentas were examined for each case where available. Main outcome measures Presence of established and/or recent brain damage. Results Clinical details were available for 471 stillborn fetuses, and detailed neuropathology was possible in 191 cases. Of these 191, 13 were multiple births, 9 died following abruption, 12 were intrapartum deaths and 157 were antepartum stillborn fetuses (99 preterm and 58 full term). Recent or established brain damage was seen in 66% of the entire cohort. Thirty‐five percent of all cases showed well‐established hypoxic damage predating the last evidence of fetal life, and this was more common in preterm fetuses ( P = 0.015), those fetuses with evidence of recent damage ( P < 0.001), in pregnancies complicated by pregnancy‐induced hypertension ( P = 0.044) and those in whom the placenta was <10th centile ( P = 0.002). Conclusions Brain damage is commonly seen in stillborn infants, and in around one‐third of cases, damage predates the period immediately before death. Factors suggesting suboptimal placental function are associated with such damage. Early identification of placental impairment may lead to improved pregnancy outcome.