Falls in oxygen saturations accompany electrographic seizures in term neonates: an observational study.

BACKGROUND: Effective seizure detection is important however, clinical signs of seizure activity may be subtle in neonates. This study aimed to systematically investigate SpO2 and respiratory pattern changes associated with EEG seizures in term-born neonates. METHOD: An observational study in term neonates at risk of seizures admitted to a single tertiary level neonatal intensive care unit. Synchronised high-resolution physiological data (ECG, pulse oximetry, respiration) and EEG/amplitude-integrated EEG (aEEG) monitoring were recorded. Sections of traces with evidence of clear EEG seizure activity were compared with physiological data recorded at the same time. RESULTS: 22/44 (50%) neonates who had aEEG monitoring were noted to have electrographic seizures. Physiologic download measurements were available for 11 of these neonates. In nine of these, an acute drop in oxygen saturation (SpO2) of at least 5% was noted in at least one seizure. Accompanying apnoeas were noted in three neonates. CONCLUSION: Acute decreases in SpO2 were seen in term neonates associated with seizures and these were not always accompanied by an apnoeic episode. Physiologic download in association with EEG monitoring may assist in improving seizure detection. Unexplained drops in SpO2 could indicate further investigation for possible seizures in at-risk neonates. IMPACT: A decrease in blood oxygen saturation (SpO2) associated with EEG seizures can occur in term infants with HIE or perinatal stroke. Drops in SpO2 associated with EEG seizures in term infants with HIE or stroke may occur in the absence of apnoeas. Unexplained acute falls in SpO2 in sick neonates may suggest possible seizures. Drops in SpO2 associated with seizures in term infants can occur over less than 3 minutes. Physiological monitoring alongside EEG monitoring could help to improve seizure detection.

Transferring preterm infants into an open cot using a heated mattress at ≤ 1400 g.

OBJECTIVE: The objective of this study is to evaluate the corrected age and weight that infants were transferred into an open cot using a heated mattress, in overall and within the subgroups of early (weight ≤ 1400 g) and standard transfer (weight > 1400 g). DESIGN: Retrospective cohort study in a tertiary neonatal unit RESULTS: One hundred and thirty-five preterm infants were analysed. The mean weight of moving into an open cot was 1370 ± 167 g at a corrected age 33 ± 1.8 weeks. Eighty-three infants (61%) were transferred early at a mean weight 1276 ± 98 g compared with 52 infants of standard transfer with a mean weight 1522 ± 141 g. Infants of the early group had higher weight gain, were discharged earlier and had shorter length of stay. CONCLUSIONS: Stable preterm infants can be safely moved to an open cot at < 33 weeks and weight ≤ 1400 g.

Whole Blood Gene Expression Reveals Specific Transcriptome Changes in Neonatal Encephalopathy.

BACKGROUND: Variable responses to hypothermic neuroprotection are related to the clinical heterogeneity of encephalopathic babies; hence better disease stratification may facilitate the development of individualized neuroprotective therapies. OBJECTIVES: We examined if whole blood gene expression analysis can identify specific transcriptome profiles in neonatal encephalopathy. MATERIAL AND METHODS: We performed next-generation sequencing on whole blood RNA from 12 babies with neonatal encephalopathy and 6 time-matched healthy term babies. Genes significantly differentially expressed between encephalopathic and control babies were identified. This set of genes was then compared to the host RNA response in septic neonates and subjected to pathway analysis. RESULTS: We identified 950 statistically significant genes discriminating perfectly between healthy controls and neonatal encephalopathy. The major pathways in neonatal encephalopathy were axonal guidance signaling (p = 0.0009), granulocyte adhesion and diapedesis (p = 0.003), IL-12 signaling and production in macrophages (p = 0.003), and hypoxia-inducible factor 1α signaling (p = 0.004). There were only 137 genes in common between neonatal encephalopathy and bacterial sepsis sets. CONCLUSION: Babies with neonatal encephalopathy have striking differences in gene expression profiles compared with healthy control and septic babies. Gene expression profiles may be useful for disease stratification and for developing personalized neuroprotective therapies.