Brain injury and intrauterine death

Sims, Maureen E.; Turkel, Susan Beckwitt; Halterman, George; Paul, Richard H.

doi:10.1016/0002-9378(85)90503-4

Cited by 75 publications

(30 citation statements)

References 3 publications

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“…The excess of brain damage in immature stillborn infants has been noted by others, 32,41 and in this cohort, it was most common in those preterms with growth restriction, where fetal compromise had been long-standing. Studies of the effects of PIH on the fetus and newborn are conflicting: PIH leads to uteroplacental vascular disease and reduced perfusion of the fetus, resulting in chronic growth restriction and acidosis.…”

Section: Clinicopathological Correlationmentioning

confidence: 93%

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The Scottish Perinatal Neuropathology Study—clinicopathological correlation in stillbirths

Becher

Bell

et al. 2006

BJOG

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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, 1995Scotland, -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.

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Section: Clinicopathological Correlationmentioning

confidence: 93%

“…13,31,32 Over one-third of our cohort showed evidence of established hypoxic changes, suggesting damage of at least 1-or 2-day duration. In addition, some of the white matter changes suggested damage of longer duration sustained several days before demise.…”

Section: Neuropathologymentioning

confidence: 99%

The Scottish Perinatal Neuropathology Study—clinicopathological correlation in stillbirths

Becher

Bell

et al. 2006

BJOG

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“…Post mortem studies indicate that hypoxic-ischemic and asphyxic episodes can significantly contribute to brain injury, morbidity and mortality (Low, 2004;Low et al, 1989;Sims et al, 1985). Late in gestation, hypoxia-ischemia predominantly results in injury of cortical gray matter, thalamic nuclei, subcortical hemorrhage and intraventricular hemorrhage to a lesser extent (Counsell et al, 2010;Cowan et al, 2003;Van den Broeck et al, 2007).…”

Section: Introductionmentioning

confidence: 93%

Morphological evaluation of the cerebral blood vessels in the late gestation fetal sheep following hypoxia in utero

Baburamani¹,

Lo²,

Castillo‐Melendez³

et al. 2013

Microvascular Research

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“…The neuropathology of perinatal death has been described both in classic and recent studies [1][2][3][4][5][6][7][8][9][10], but most of these do not clearly separate live born from stillborn infants and relatively few are devoted solely to stillbirths [9,[11][12][13][14][15][16][17]. However, there is sufficient evidence in the literature to show that most if not all of the lesions seen in neonates may also be found in the brains of stillborn foetuses [3,7,9,12].…”

Section: Introductionmentioning

confidence: 95%

The neuropathology of stillbirth — Correlation with apolipoprotein genotype in a Scottish population based study

Bell¹,

Becher²,

Keeling³

et al. 2015

Early Human Development

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Brain injury and intrauterine death

Cited by 75 publications

References 3 publications

The Scottish Perinatal Neuropathology Study—clinicopathological correlation in stillbirths

The Scottish Perinatal Neuropathology Study—clinicopathological correlation in stillbirths

Morphological evaluation of the cerebral blood vessels in the late gestation fetal sheep following hypoxia in utero

The neuropathology of stillbirth — Correlation with apolipoprotein genotype in a Scottish population based study

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