In this single centre cohort study, marked improvements in survival over a 20-year period were not accompanied by a significant increase in neurodevelopmental morbidity.

Whole-body hypothermia for 24 hours at either 35 or 33 degrees C, commenced 2 hours after resuscitation, prolonged the NTP/EPP latent phase and reduced the overall secondary falls in mean PCr/Pi and NTP/EPP during 48 hours after HI. Reducing the temperature from 35 to 33 degrees C neither increased mean PCr/Pi and NTP/EPP nor further lengthened the latent phase.

Hypothermia after perinatal hypoxia-ischemia (HI) is neuroprotective; the precise brain temperature that provides optimal protection is unknown. To assess the pattern of brain injury with 3 different rectal temperatures, we randomized 42 newborn piglets: (Group i) sham-normothermia (38.5-39 degrees C); (Group ii) sham-33 degrees C; (Group iii) HI-normothermia; (Group iv) HI-35 degrees C; and (Group v) HI-33 degrees C. Groups iii through v were subjected to transient HI insult. Groups ii, iv, and v were cooled to their target rectal temperatures between 2 and 26 hours after resuscitation. Experiments were terminated at 48 hours. Compared with normothermia, hypothermia at 35 degrees C led to 25 and 39% increases in neuronal viability in cortical gray matter (GM) and deep GM, respectively (both p < 0.05); hypothermia at 33 degrees C resulted in a 55% increase in neuronal viability in cortical GM (p < 0.01) but no significant increase in neuronal viability in deep GM. Comparing hypothermia at 35 and 33 degrees C, 35 degrees C resulted in more viable neurons in deep GM, whereas 33 degrees C resulted in more viable neurons in cortical GM (both p < 0.05). These results suggest that optimal neuroprotection by delayed hypothermia may occur at different temperatures in the cortical and deep GM. To obtain maximum benefit, you may need to design patient-specific hypothermia protocols by combining systemic and selective cooling.

This study investigated whether in preterm children who had ventricular dilatation (VD) on neonatal cranial ultrasound outcome at age 8 years was influenced by the additional presence of germinal matrix haemorrhage -intraventricular haemorrhage (GMH-IVH). Six-hundred and ninety-nine preterm infants (<33wks' gestation, mean 29.6wks [SD 2.1]) with either normal cranial ultrasound (n=616; 286 females, 330 males), or with VD with (n=66; 32 females, 34 males) or without (n=17; 4 females, 13 males) GMH-IVH were enrolled in the study. At age 8 years outcome was assessed in 567 (81%) of the 699 children by neurological examination, the Test of Motor Impairment (TOMI), the test of Visuo-Motor Integration (VMI), and the Wechsler Intelligence Scales for Children. Results showed that the proportion of children with disabling impairments was higher in the group with VD and GMH-IVH. Performance on TOMI and VMI (even in those without disabling impairments) was poorer in those with VD and GMH-IVH than in children with normal scans or those with VD only. Children with VD and GMH-IVH had significantly lower performance IQ than children with normal ultrasound, whereas those with VD only were not different from those with normal scans. Results suggest the presence of subtle white matter injury that has not been identified by neonatal cranial ultrasound. Although this study did not investigate biochemical markers of haemorrhage, we hypothesize that non-proteinbound iron is likely to be a contributing factor to white matter damage in preterm infants.

Aim: To determine cerebral blood flow using near infrared spectroscopy in extremely preterm infants undergoing high‐frequency oscillatory ventilation during the first three days of life. Low cerebral blood flow has been associated with both intra‐ventricular haemorrhage and periventricular leucomalacia. It is well established that cerebral blood flow increases over the first three days of life in extremely preterm infants who are conventionally ventilated with intermittent positive pressure ventilation. However, there is no information about cerebral blood flow in preterm babies undergoing high‐frequency oscillatory ventilation. In addition, there are concerns that high‐frequency oscillatory ventilation may be associated with an increased incidence of intra‐ventricular haemorrhage in premature infants. Methods: Thirteen appropriately grown, preterm infants of less than 28 wk gestation who were admitted to the neonatal unit at University College Hospital, London were studied using near infrared spectroscopy. Left ventricular output and right ventricular output were assessed echocardiographically. Results: Extremely preterm infants undergoing high‐frequency oscillatory ventilation have remarkably low cerebral blood flow in the first 12 h of life, median 6.7 (range 4.4‐11) mls. 100 g−1min−1 followed by an increase over the subsequent three days. Left ventricular output also increased over the first three days of life, whereas right ventricular output showed no clear relationship with time. Despite low cerebral blood flow only one infant had evidence of major cerebral injury. Conclusion: Cerebral blood flow is extremely low in this group of preterm babies. Despite this extremely low cerebral blood flow, the clinical outcome is good. There was an increase in cerebral blood flow and a corresponding increase in left ventricular output over the first few days of life.