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

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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.

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