Cerebral palsy and neonatal encephalopathy.

Gaffney, G; Flavell, V; Johnson, Ann; Squier, M. V.; Sellers, Susan

doi:10.1136/fn.70.3.f195

Cited by 83 publications

(45 citation statements)

References 38 publications

(13 reference statements)

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“…35 When exposure to labor is avoided by the use of an elective pre-labor CD, the occurrence of HIE virtually disappears. 11,36,37 Although there were clear differences in intrapartum factors between cases and controls, there were few that were apparent early enough to lead to differences in management that might have reduced the number of infants who had HIE. The association between HIE and intrapartum factors does not necessarily imply that this condition is caused by poor care during labor.…”

Section: Figurementioning

confidence: 99%

Antepartum and Intrapartum Factors Preceding Neonatal Hypoxic-Ischemic Encephalopathy

et al. 2013

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WHAT'S KNOWN ON THIS SUBJECT: Etiology and timing of onset of neonatal hypoxic-ischemic encephalopathy continue to be controversial. Previous studies suggest antepartum events are the main contributing factors, but have used a broad definition of encephalopathy and included infants with genetic, congenital, and developmental abnormalities.WHAT THIS STUDY ADDS: Our study suggests that when strict criteria defining hypoxic-ischemic encephalopathy are applied with supporting neuroimaging evidence of an acute hypoxicischemic insult, intrapartum events are the final and necessary pathway leading to this condition. abstract OBJECTIVE: To determine whether antepartum factors alone, intrapartum factors alone, or both in combination, are associated with term neonatal hypoxic-ischemic encephalopathy (HIE). METHODS:A total of 405 infants $35 weeks' gestation with early encephalopathy, born between 1992 and 2007, were compared with 239 neurologically normal infants born between 1996 and 1997. All cases met criteria for perinatal asphyxia, had neuroimaging findings consistent with acute hypoxia-ischemia, and had no evidence for a non-hypoxic-ischemic cause of their encephalopathy.RESULTS: Both antepartum and intrapartum factors were associated with the development of HIE on univariate analysis. Case infants were more often delivered by emergency cesarean delivery (CD; 50% vs 11%, P , .001) and none was delivered by elective CD (vs 10% of controls). On logistic regression analysis only 1 antepartum factor (gestation $41 weeks) and 7 intrapartum factors (prolonged membrane rupture, abnormal cardiotocography, thick meconium, sentinel event, shoulder dystocia, tight nuchal cord, failed vacuum) remained independently associated with HIE (area under the curve 0.88; confidence interval 0.85-0.91; P , .001). Overall, 6.7% of cases and 43.5% of controls had only antepartum factors; 20% of cases and 5.8% of controls had only intrapartum factors; 69.5% of cases and 31% of controls had antepartum and intrapartum factors; and 3.7% of cases and 19.7% of controls had no identifiable risk factors (P , .001). CONCLUSIONS:Our results do not support the hypothesis that HIE is attributable to antepartum factors alone, but they strongly point to the intrapartum period as the necessary factor in the development of this condition. Pediatrics 2013;132:e952-e959

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Section: Figurementioning

confidence: 99%

Antepartum and Intrapartum Factors Preceding Neonatal Hypoxic-Ischemic Encephalopathy

et al. 2013

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“…A second difficulty is the lack of a standard definition of what constitutes a birth defect and which defects are regarded as major or minor. Some studies have chosen, for example, to exclude major birth defects (Gaffney et al 1994) without defining what constitutes a major defect.…”

Section: Discussionmentioning

confidence: 99%

“…Most previous studies have included only those infants thought to have had intrapartum hypoxia, and most have either excluded infants with birth defects (Ziegler et al 1976, Finer et al 1981, Low et al 1985, Robertson and Finer 1985, Gaffney et al 1994, Thornberg et al 1995 or have not mentioned whether infants with birth defects had been included or excluded (Levene et al 1985, Hull andDodd 1992). Furthermore, in the studies that excluded birth defects, the definition was not always clear or consistent across studies, with most papers defining birth defects as 'malformations', or 'major malformations'.…”

mentioning

confidence: 99%

“…Furthermore, in the studies that excluded birth defects, the definition was not always clear or consistent across studies, with most papers defining birth defects as 'malformations', or 'major malformations'. For example, Ziegler and colleagues (1976) excluded children with malformations and embryopathy, Low and coworkers (1985) excluded genetically determined and CNS anomalies and Gaffney and colleagues excluded major malformations (Gaffney et al 1994). Amiel-Tison excluded trisomies and obvious congenital malformations (Amiel-Tison 1969), Finer and coworkers excluded infants with CNS and chromosomal anomalies or familial illness (Finer et al 1981), Thornberg and coworkers excluded congenital malformations, chromosomal disorders, and congenital neuromuscular disorders (Thornberg et al 1995), and Robertson and Finer excluded all children with known syndromes or malformations affecting the CNS (Robertson and Finer.…”

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confidence: 99%

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Birth defects in children with newborn encephalopathy

Felix

Badawi

Kurinczuk

et al. 2000

Develop Med Child Neuro

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This study was designed to investigate birth defects found in association with newborn encephalopathy. All possible birth defects were ascertained in a population‐based study of 276 term infants with moderate or severe encephalopathy and 564 unmatched term control infants. A strong association between birth defects and newborn encephalopathy was found with defects affecting 27.5% of children with encephalopathy and 4.3% of control children (odds ratio 8.55; 95% confidence interval 5.25 to 13.91; p<0.001). In 11.8% of infants with a birth defect the defect was not diagnosed until after the newborn period, illustrating one of the difficulties in attempting to exclude infants with birth defects from studies of newborn encephalopathy. The majority of defects (89%) were not specific anomalies of the CNS. In 36.8% of children with encephalopthy who had a birth defect, the defect was considered to be the probable cause of the encephalopathy. Infants with birth defects who had encephalopathy had a poorer prognosis than those without: they were twice as likely to die by the age of 2 years and three times more likely to have cerebral palsy. This study catalogues the spectrum of birth defects associated with newborn encephalopathy and illustrates the importance of their inclusion when investigating both the aetiology and outcome of this condition.

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“…Cases comprised all children born in the English counties of Oxfordshire, Berkshire and Northamptonshire between 1990-1993 with a diagnosis of cerebral palsy (ICD-9 classification) that were identified from the populationbased Oxford Register of Early Childhood Impairment (Gaffney et al, 1994). The date of birth and surname of the case were used to locate the delivery register entry of the individual's birth and the information recorded there was used to identify the mothers' obstetric records, including ultrasound reports.…”

Section: Methodsmentioning

confidence: 99%

A Case-control Study of Vanishing Twin as a Risk Factor for Cerebral Palsy

Newton

Casabonne

Johnson³

et al. 2003

Twin res.

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It has been hypothesized that cerebral palsy of unknown etiology is the result of the death of an unrecognized co-twina vanishing twin -in early gestation. We conducted a casecontrol study of vanishing twin as a risk factor for cerebral palsy of unknown etiology in women who had an obstetric ultrasound during pregnancy. Among mothers of cases, one of 86 had evidence of a vanishing twin on ultrasound, as compared to two of 381 control mothers (odds ratio [OR] 2.2, 95% confidence interval [CI] 0.2-24.8; p = 0.5). Bleeding in early pregnancy, which may indicate the loss of a co-twin, was reported by 14 case mothers and 46 control mothers (OR 1.6, 95% CI 0.8-3.0; p = 0.3). On the basis of results presented here, the vanishing twin syndrome is unlikely to account for a high proportion of cases of cerebral palsy, but there is insufficient statistical power to draw firm conclusions.The introduction of obstetric ultrasound scanning has drawn attention to the vanishing twin syndrome in which more than one fetus, or fetal sac, is observed early in gestation, whereas at delivery, there is a singleton birth. Pharoah and Cooke (1997) have hypothesized that the death of a co-twin in early gestation (less than 12 weeks) may put the surviving twin at risk of spastic cerebral palsy and could account for the majority of cases of cerebral palsy of unknown cause. The proportion of pregnancies demonstrating the vanishing twin phenomenon depends on the definition used. Landy and colleagues (1986) identified 7 out of 1000 pregnancies in which 2 sacs were demonstrated on ultrasound prior to 12 weeks gestation, both with fetal heart movements, followed by a single fetus at later gestation. Fetal loss occurred within 2 weeks of the first scan and was usually accompanied by vaginal bleeding. Using a broader definition of vanishing twin, encompassing the presence of an empty sac on ultrasound with no fetal heart pulsation detected, Landy et al. identified 24 out of a 1000 pregnancies demonstrating the phenomenon. In order to test the hypothesis that vanishing twin is a cause of cerebral palsy of unknown etiology, we conducted a case-control study in women who had an obstetric ultrasound scan during pregnancy. Materials and MethodsCases comprised all children born in the English counties of Oxfordshire, Berkshire and Northamptonshire between 1990-1993 with a diagnosis of cerebral palsy (ICD-9 classification) that were identified from the populationbased Oxford Register of Early Childhood Impairment (Gaffney et al., 1994). The date of birth and surname of the case were used to locate the delivery register entry of the individual's birth and the information recorded there was used to identify the mothers' obstetric records, including ultrasound reports. Four controls per case were identified from the delivery register matched for date of birth, sex and hospital of birth; these comprised the two individuals of the same sex born just before the case and the two born just after the case. Because information was obtained from obstetric records, r...

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Cerebral palsy and neonatal encephalopathy.

Abstract: 95%

Cited by 83 publications

References 38 publications

Antepartum and Intrapartum Factors Preceding Neonatal Hypoxic-Ischemic Encephalopathy

Antepartum and Intrapartum Factors Preceding Neonatal Hypoxic-Ischemic Encephalopathy

Birth defects in children with newborn encephalopathy

A Case-control Study of Vanishing Twin as a Risk Factor for Cerebral Palsy

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