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dc.contributor.authorMurray, Deirdre M
dc.contributor.authorO'Riordan, Mairead N
dc.contributor.authorHorgan, Richard
dc.contributor.authorBoylan, Geraldine
dc.contributor.authorHiggins, John R
dc.contributor.authorRyan, Cornelius A
dc.date.accessioned2012-01-09T15:53:53Z
dc.date.available2012-01-09T15:53:53Z
dc.date.issued2009-09
dc.identifier.citationFetal heart rate patterns in neonatal hypoxic-ischemic encephalopathy: relationship with early cerebral activity and neurodevelopmental outcome. 2009, 26 (8):605-12 Am J Perinatolen
dc.identifier.issn1098-8785
dc.identifier.pmid19399706
dc.identifier.doi10.1055/s-0029-1220774
dc.identifier.urihttp://hdl.handle.net/10147/200952
dc.description.abstractDespite widespread use of fetal heart rate monitoring, the timing of injury in hypoxic-ischemic encephalopathy (HIE) remains unclear. Our aim was to examine fetal heart rate patterns during labor in infants with clinical and electroencephalographic (EEG) evidence of HIE and to relate these findings to neurodevelopmental outcome. Timing of onset of pathological cardiotocographs (CTGs) was determined in each case by two blinded reviewers and related to EEG grade at birth and neurological outcome at 24 months. CTGs were available in 35 infants with HIE (17 mild, 12 moderate, 6 severe on EEG). Admission CTGs were normal in 24/35 (69%), suspicious in 8/35 (23%), and pathological in 3/35 (8%). All CTGs developed nonreassuring features prior to delivery. Three patterns of fetal heart rate abnormalities were seen: group 1, abnormal CTGs on admission in 11/35 (31%); group 2, normal CTGs on admission with gradual deterioration to pathological in 20/35 cases (57%); and group 3, normal CTGs on admission with acute sentinel events in 4/35 (11.5%). The median (interquartile range) duration between the development of pathological CTGs and delivery was 145 (81, 221) minutes in group 2 and 22 (12, 28) minutes in group 3. There was no correlation between duration of pathological CTG trace and grade of encephalopathy (R = 0.09, P = 0.63) or neurological outcome (P = 0.75). However, the grade of encephalopathy was significantly worse in group 3 (P = 0.001), with a trend to worse outcomes. The majority of infants with HIE have normal CTG traces on admission but develop pathological CTG patterns within hours of delivery. More severe encephalopathy was associated with normal admission CTG and acute sentinel events shortly before delivery.
dc.language.isoenen
dc.publisherThieme Publicationsen
dc.subject.meshCardiotocography
dc.subject.meshChild Development
dc.subject.meshElectroencephalography
dc.subject.meshFetal Monitoring
dc.subject.meshHeart Rate, Fetal
dc.subject.meshHumans
dc.subject.meshHypoxia-Ischemia, Brain
dc.subject.meshInfant
dc.subject.meshInfant, Newborn
dc.subject.meshNeurologic Examination
dc.subject.meshSeizures
dc.titleFetal heart rate patterns in neonatal hypoxic-ischemic encephalopathy: relationship with early cerebral activity and neurodevelopmental outcome.en
dc.typeArticleen
dc.contributor.departmentDepartment of Paediatrics and Child Health, University College Cork, Cork University Maternity Hospital, Cork, Wilton, Cork, Ireland. d.murray@ucc.ieen
dc.identifier.journalAmerican journal of perinatologyen
dc.description.provinceMunster
html.description.abstractDespite widespread use of fetal heart rate monitoring, the timing of injury in hypoxic-ischemic encephalopathy (HIE) remains unclear. Our aim was to examine fetal heart rate patterns during labor in infants with clinical and electroencephalographic (EEG) evidence of HIE and to relate these findings to neurodevelopmental outcome. Timing of onset of pathological cardiotocographs (CTGs) was determined in each case by two blinded reviewers and related to EEG grade at birth and neurological outcome at 24 months. CTGs were available in 35 infants with HIE (17 mild, 12 moderate, 6 severe on EEG). Admission CTGs were normal in 24/35 (69%), suspicious in 8/35 (23%), and pathological in 3/35 (8%). All CTGs developed nonreassuring features prior to delivery. Three patterns of fetal heart rate abnormalities were seen: group 1, abnormal CTGs on admission in 11/35 (31%); group 2, normal CTGs on admission with gradual deterioration to pathological in 20/35 cases (57%); and group 3, normal CTGs on admission with acute sentinel events in 4/35 (11.5%). The median (interquartile range) duration between the development of pathological CTGs and delivery was 145 (81, 221) minutes in group 2 and 22 (12, 28) minutes in group 3. There was no correlation between duration of pathological CTG trace and grade of encephalopathy (R = 0.09, P = 0.63) or neurological outcome (P = 0.75). However, the grade of encephalopathy was significantly worse in group 3 (P = 0.001), with a trend to worse outcomes. The majority of infants with HIE have normal CTG traces on admission but develop pathological CTG patterns within hours of delivery. More severe encephalopathy was associated with normal admission CTG and acute sentinel events shortly before delivery.


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