In this prospective cerebral hemodynamic index study using doppler ultrasonography done in hemodynamically stable neonates born between 28 0/6 to 34 6/7 weeks in SGA and AGA neonates during the first 72 hours of life. It was found pulsatility index and resistive index were significantly lower in SGA neonates as compared to AGA neonates in middle cerebral artery dopplers.
Pulsatility index (PI) is defined as the difference between the peak systolic flow and minimum diastolic flow velocity, divided by the mean velocity recorded throughout the cardiac cycle[5]. It is a non-invasive easily obtainable method of assessing vascular resistance with the use of Doppler ultrasonography. The median (IQR) pulsatility index (PI) was lower in SGA neonates 1.12 (1.01-1.32) vs 1.28 (1.10-1.51) in AGA neonates, p = 0.05 on day 3 in the MCA. Both SGA and AGA neonates had similar cardiac indices and no HSPDA during the study period. A lower PI among the SGA neonates possibly reflects the continuation of in-utero phenomenon of redistribution of cardiac output to the brain secondary to cerebral vasodilatation[6]. Krishnamurthy et al, compared 20 SGA neonates with AGA neonates in a gestation range from 26-37 weeks and found significantly lower PI in the SGA neonates in the first few days. A recent systematic review found insufficient evidence to support the use of pulsatility index to predict brain injury and long term neurodevelopmental outcomes[7].
Resistive index (RI) is a marker of cerebral vascular autoregulation is less prone to errors related to the angle of insonation between the vessel and the doppler ultrasound beam. RI basically is a measure of end organ resistance [8]. In the present study, mean ± SD RI was significantly lower 0.68 ± 0.07 in SGA neonates vs 0.72 ± 0.08, in AGA neonates p = 0.01 in the cerebral dopplers of MCA on day 3 which probably reflects the redistribution of blood flow to the brain in IUGR neonates. Low RI reflects the pressure passive blood flow and can be a surrogate marker of autoregulatory dysregulation. Postnatal continuation of the increased cerebral blood flow might cause hyperoxia, which may trigger a burst of free reactive oxygen species [1].
Krishnamurthy et al, found significantly lower RI in the SGA neonates in the first few days life[4]. Montaldo et al, compared RI in ACA in 100 term SGA with IUGR and AGA neonates during the first 72 hours and found that RI was significantly lower in SGA growth restricted fetuses at 6 and 24 hours, however there was no difference in RI at 48 and 72 hours [1].
Of note, postnatal changes in cerebral blood flow velocity have been suggested as prognostic markers for adverse neurodevelopment in IUGR neonates. Argollo et al. demonstrated that abnormal RI values within 72 h of birth was associated with complications of neonates with white matter injury[9]. However , the predictive value of RI in predicting brain injury and long term neurodevelopmental outcomes is not well established[7]. Since our population was non sick neonates whether these subclinical alterations of cerebral doppler indices among premature SGA neonates translate into long term impaired neurological outcomes should be further studied.
Strengths of the study includes that hemodynamically stable non sick neonates were included in the study providing a step in the direction of generating a data for normative references and cerebral dopplers offer an easy to access, inexpensive and practical tool for the non-invasive evaluation of cerebral hemodynamics. Majority of the images (95%) were captured by a single investigator, which decreased the chances of interobserver bias. For quality assurance, the images were reviewed by senior radiologist on a weekly basis. Moreover, the images were taken at 3 time points sequentially for better understanding of transitional circulation. And being an inborn institute, all of the antenatal, natal and postnatal factors were uniform and standardized across the unit.
We suggest for a similar study with larger sample size with multiple centres across different demographic population adequately powered should further be planned to generate age and gestation specific normograms.
To conclude cerebral hemodynamics is different in preterm SGA and AGA neonates and growth restriction has a direct impact on cerebral hemodynamics. Furthermore, this subclinical altered cerebral hemodynamics in SGA neonates whether it translates into impaired neurodevelopmental outcomes should be further studied.