ABSTRACT
Despite 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.
KEYWORDS
Neonatal - hypoxic-ischemic encephalopathy - electroencephalography - cardiotocograph
- neurological outcome
REFERENCES
- 1 Volpe J J. Neurology of the Newborn 2001. 4th ed. Philadelphia; WB Saunders 2001
- 2 Thacker S B, Stroup D F. Continuous electronic fetal monitoring versus intermittent
auscultation for assessment during labour. Cochrane review 1999; The Cochrane Library.
Issue No. 1. Oxford; update software 1999
- 3
Nelson K B, Dambrosia J M, Ting T Y, Grether J K.
Uncertain value of electronic fetal monitoring in predicting cerebral palsy.
N Engl J Med.
1996;
334
613-618
- 4
Spencer J A, Badawi N, Burton P, Keogh J, Pemberton P, Stanley F.
The intrapartum CTG prior to neonatal encephalopathy at term: a case-control study.
Br J Obstet Gynaecol.
1997;
104
25-28
- 5
Schifrin B S, Hamilton-Rubenstein T, Shields J R.
Fetal heart rate patterns and the timing of fetal injury.
J Perinatol.
1994;
14
174-181
- 6
Skupski D W, Rosenberg C R, Eglinton G S.
Intrapartum fetal stimulation tests: a meta-analysis.
Obstet Gynecol.
2002;
99
129-134
- 7
Nelson K B, Ellenberg J H.
Antecedents of cerebral palsy. Multivariate analysis of risk.
N Engl J Med.
1986;
315
81-86
- 8
Westgate J A, Gunn A J, Gunn T R.
Antecedents of neonatal encephalopathy with fetal acidaemia at term.
B J Obstet Gynaecol.
1999;
106
774-782
- 9
van Lieshout H BM, Jacobs J WFM, Rotteveel J J, Geven W, v't Hof M.
The prognostic value of the EEG inasphyxiated newborns.
Acta Neurol Scand.
1995;
91
203-205
- 10
Takeuchi T, Watanabe K.
The EEG evolution and neurological prognosis of neonates with perinatal hypoxia.
Brain Dev.
1989;
11
115-120
- 11
Amiel-Tison C.
Update of the Amiel-Tison neurological assessment for the term neonate or at 40 weeks
corrected age.
Pediatr Neurol.
2002;
27
196-212
- 12
Pressler R M, Boylan G B, Morton M, Binnie C D, Rennie J M.
Early serial EEG in hypoxic ischaemic encephalopathy.
Clin Neurophysiol.
2001;
112
31-37
- 13
Sarnat H B, Sarnat M S.
Neonatal encephalopathy following foetal distress: a clinical and electroencephalographic
study.
Arch Neurol.
1976;
33
696-705
- 14 Griffiths R. The Abilities of Babies. London; University of London Press 1954
- 15
Cowan F, Rutherford M, Groenendaal F et al..
Origin and timing of brain lesions in term infants with neonatal encephalopathy.
Lancet.
2003;
361
736-742
- 16
Phelan J P, Ahn M O.
Perinatal observations in forty-eight neurologically impaired term infants.
Am J Obstet Gynecol.
1994;
171
424-431
- 17
Phelan J P, Ahn M O.
Fetal heart rate observations in 300 term brain-damaged infants.
J Matern Fetal Investig.
1998;
8
1-5
- 18
Barnett A, Mercuri E, Rutherford M et al..
Neurological and perceptual-motor outcome at 5–6 years of age in children with neonatal
encephalopathy.
Neuropediatrics.
2002;
33
242-248
- 19
MacLennan A.
A template for defining a causal relationship between acute intrapartum events and
cerebral palsy: international consensus statement.
BMJ.
1999;
319
1054-1059
- 20
Myers R E.
Fetal asphyxia due to umbilical cord compression. Metabolic and brain pathologic consequences.
Biol Neonate.
1975;
26
21-43
- 21
Pasternak J F, Gorey M T.
The syndrome of acute near total intrauterine asphyxia in the term infant.
Pediatr Neurol.
1998;
18
391-398
- 22
Murray D M, Boylan G B, Ryan C A, Connolly S.
Early continuous video-EEG in acute near-total intrauterine asphyxia.
Pediatr Neurol.
2006;
35
52-56
- 23
Ikeda T, Murata Y, Quilligan E J, Parer J T et al..
Fetal heart rate patterns in postasphyxiated fetal lambs with brain damage.
Am J Obstet Gynecol.
1998;
179
1329-1337
- 24
Dellinger E H, Boehm F H, Crane M M.
Electronic fetal heart rate monitoring: early neonatal outcomes associated with normal
rate, fetal stress, and fetal distress.
Am J Obstet Gynecol.
2000;
182
214-220
- 25
Badawi N, Kurinczuk J J, Keogh J M et al..
Antepartum risk factors for newborn encephalopathy: the western Australian case-control
study.
BMJ.
1998;
317
1549-1553
- 26
Badawi N, Kurinczuk J J, Keogh J M et al..
Intrapartum risk factors for newborn encephalopathy: the western Australian case-control
study.
BMJ.
1998;
317
1554-1558
Dr. Deirdre Murray
Department of Paediatrics and Child Health, Clinical Investigations Unit
Cork University Hospital, Wilton, Cork, Ireland
eMail: d.murray@ucc.ie