Using range-gated pulsed Doppler sonography, cerebral blood flow velocity (CBFV) waveforms from the anterior cerebral artery (ACA), middle cerebral artery (MCA) and circle of Willis artery (CW) were examined in a total of 34 newborn infants. We compared the pulsatility index (PI) from the three cerebral arteries sampled in 10 term and 10 preterm (29 +/- 2 weeks) newborn infants without a history of perinatal asphyxia or intracranial pathology. The Pl in the ACA ranged from 0.60 to 1.03. There were no significant differences in Pl between the three vessels by paired comparisons. The Pl of the MCA differed from that of the ACA by 0.00 +/- 0.05. The variation coefficient (CV) was 7%. For CW with ACA, the difference was 0.00 +/- 0.04 and CV was 6%. Both intra- and interexaminer variation in Pl measurements were studied in another 14 infants. The variation coefficients were 5-8% for all three cerebral arteries. We showed that CBFV waveform patterns were similar in regional cerebral arteries, with Pl being a consistent CBFV index. In normal cerebral circulation, the intervessel Pl differences were within observer variations. Deviation from this may suggest abnormal regional cerebral haemodynamics.

To evaluate the effect of ventricular dilation (VD) on cerebral hemodynamics, serial cerebral bloodflow velocity patterns from the anterior and middle cerebral, and circle of Willis arteries were examined by range-gated, pulsed Doppler sonography in premature infants developing post-hemorrhagic VD. Nine infants (25 to 30 weeks gestation) without a patent ductus arteriosus were studied until resolution of VD. Forty-nine cranial sonograms from all nine infants were reviewed independently and grouped cross-sectionally into mild, moderate and severe VD prior to shunt. The corresponding pulsatility index (PI) showed a consistent trend of increase with VD in all three studied vessels. In six infants, absent or reversed diastolic flow was observed at the height of VD. Four of these infants required V-P shunt. Immediate fall in PI occurred in all three vessels. Serial measurement of PI during VD reflects global changes in cerebrovascular resistance. Results confirmed PI could be a useful index in monitoring cerebral hemodynamic changes.

Cranial ultrasound (US) has not been considered useful in the assessment of FT asphyxia. 31 infants with at least 2 of the following were evaluated: fetal distress, Apgar ≤5 at 1 or 5 min, need for immediate resuscitation and abnormal neurological examination in 1st 24 hrs. One infant with only latter finding was included. All infants had at least 1 US in 1st 7 days. US revealed 2 major patterns of abnormality, diffuse and focal. The severity of asphyxia was graded by clinical and EEC criteria. In B & C 7/13 normal US were done on day 1 or 2 and 4/13 with only small ventricles were graded normal. Diffuse changes with slit-like ventricles and loss of anatomic landmarks or diffuse ↑ in echogenicity were seen in 6 infants. Focal ↑ in echogenicity was cortical in 2 infants and in periventricular white matter in 3. US did not reveal a frontal cortical hemorrhage and 2 MCA infarcts diagnosed on CT 1 & 4 days later. The usefulness of US in FT asphyxia can be improved by repeating early normal studies if moderate or severe clinical abnormalities persist.

Autopsies of newborn infants dying <48 h after admission to an outborn referral centre were reviewed for (A) 1972/73 and (B) 1982/83. 154 autopsies in (A) and 89 in (B) were performed. Congenital Anomalies: 2 lesions accounted for >80% of deaths in this category in both periods: CHD (Hypoplastic L. heart commonest single abn) and pulmonary hypoplasia with associated conditions. Respiratory deaths occurred with similar frequency in all weight groups up to 2.5 kg in (A) with 37% <1000 gm. In (B) 87% of all early respiratory deaths were <1000 gm. The incidence of SEH-IVH in pulm. deaths was constant in both periods (42%). Asphyxia accounted for 13% of deaths in both (A) & (B); however, in (A) 6 of the 20 asphyxial deaths were in prematures while only 1 in 12 in (B) was <38 wks GA. Sepsis due to GBS occurred in 10/22 in (A) and 6/7 in (B). Group A infants were more immature (33 wks vs 36 wks) and lower Bwt. (x 2.0 kg vs 2.6 kg) than Group B. A decade of perinatal care directed at LBW infants has had a major impact on early deaths from lung disease in infants >1.0 kg, little change in incidence of lethal anomalies, and has highlighted the incidence of asphyxia and sepsis in more mature infants.