Broadband NIRS Cerebral Cytochrome-C-Oxidase Response to Anoxia Before and After Hypoxic-Ischaemic Injury in Piglets.

Gemma Bale,Alan Bainbridge,Ilias Tachtsidis,Laura Morrison,Keith St Lawrence,Matthew Kewin,Ajay Rajaram,Mamadou Diop

doi:10.1007/978-3-319-91287-5_24

Abstract

Perinatal hypoxic ischaemic (HI) encephalopathy is associated with severe neurodevelopment problems and mortality. This study uses broadband continuous-wave near-infrared spectroscopy (NIRS) to assess the early changes in cerebral oxygenation and metabolism after HI injury in an animal model using controlled anoxia events. Anoxia was induced before and 1 h after various levels of HI injury to assess the metabolic response via the changes in the oxidation state of cytochrome-c-oxidase (oxCCO), a marker of oxidative metabolism. The oxCCO responses to anoxia were classified into five categories: increase, no change, decrease, biphasic and triphasic responses. The most common response (54%) was a biphasic decrease in oxCCO. A change in the classification of the metabolic response to anoxia after HI injury indicated a severe injury, as determined by proton magnetic resonance spectroscopy, with 86% sensitivity. This shows that broadband NIRS can identify disturbances to cerebral metabolism in the first hours after severe HI injury.

Highlights

Neonatal hypoxic ischaemic encephalopathy (HIE) affects 1–2 live births per 1000 and is associated with severe neurodevelopmental problems and mortality [1]
HIE is monitored using amplitude-integrated EEG during treatment in the neonatal intensive care unit (NICU) but the current gold standard assessment of the HIE is proton magnetic resonance spectroscopy (1H MRS) [3]; this is generally performed towards the end of the first week of life, long after the ‘therapeutic window’ before secondary energy failure (SEF)
Of events, in 19% of events a triphasic change in oxidation state of cytochrome- c-oxidase (oxCCO) was seen; but the most common response was a biphasic decrease in oxCCO which occurred in 54% of events

Summary

Introduction

Neonatal hypoxic ischaemic encephalopathy (HIE) affects 1–2 live births per 1000 and is associated with severe neurodevelopmental problems and mortality [1]. After the initial hypoxic ischaemic (HI) injury, typically the cerebral metabolism recovers to normal for the first few hours of life but can deteriorate, leading to a secondary energy failure (SEF) [2]. HIE is monitored using amplitude-integrated EEG (aEEG) during treatment in the neonatal intensive care unit (NICU) but the current gold standard assessment of the HIE is proton magnetic resonance spectroscopy (1H MRS) [3]; this is generally performed towards the end of the first week of life, long after the ‘therapeutic window’ before SEF. An early (within the first 6 h after birth) continuous assessment of brain injury is sought in order to enable prompt treatment and to monitor recovery during the crucial first days following HIE.

Methods

Results

Conclusion