Gj. Mires et al., NEONATAL CEREBRAL DOPPLER FLOW VELOCITY WAVE-FORMS IN THE PRETERM INFANT WITH CEREBRAL PATHOLOGY, Early human development, 36(3), 1994, pp. 213-222
In a longitudinal study of 217 infants delivering at <37 completed wee
ks gestation, Doppler flow velocity waveforms were obtained, and resis
tance index (RI) values calculated from the middle (MCA) and anterior
(ACA) cerebral arteries during the first 10 days of life. Sixty infant
s demonstrated ultrasound evidence of cerebral pathology, of which fiv
e cases were congenital, and an additional 13 cases were complicated b
y patent ductus arteriosus during the study period. The Doppler data o
btained during the first week of life from the remaining 42 infants wh
o developed cerebral pathology, and 15 infants who had evidence of met
abolic acidosis at delivery without ultrasound evidence of cerebral pa
thology were compared with local reference data obtained from non-acid
otic infants with normal cranial ultrasound from 24 h of age. In those
infants who had evidence of minor periventricular haemorrhage alone (
Grade I/II PVH), there was no significant difference between the ACA o
r MCA RI during the study period compared with the reference data. In
those groups of infants who demonstrated major PVH (Grade III/IV) or p
ersistent periventricular flares, the ACA and MCA RI was found to be c
onsistently significantly higher than the reference group throughout t
he study period. In those infants who developed ultrasound evidence of
periventricular cystic leukomalacia (PVCL), the MCA RI was significan
tly lower than the reference data between 48 and 72 h of age, there be
ing no significant difference in the ACA RI. The Doppler findings in t
hose infants with evidence of metabolic acidosis at delivery (umbilica
l arterial pH <7.20; BD >8 mmol/l) but with normal ultrasound findings
were similar to those infants who developed PVCL, namely a significan
t fall in MCA RI between 48 and 72 h of life, with no significant diff
erence in the ACA RI during the study period. These findings suggest t
hat variable changes in cerebral vascular resistance occur with the ev
olution of, or as a consequence of the development of cerebral patholo
gy in the pre-term infant, and these changes of increased and decrease
d vascular resistance are discussed. Further investigation of the chan
ges occurring in the cerebral circulation in the early neonatal period
of infants who develop PVCL is required to clarify the vascular chang
es taking place, but if the findings of this study are confirmed, this
technique may provide a means of identifying infants at risk of devel
oping ischaemic cerebral pathology at an early stage when it may be po
ssible to initiate therapeutic intervention to limit the cerebral dama
ge.