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Review
. 2016 Oct 20:4:114.
doi: 10.3389/fped.2016.00114. eCollection 2016.

Preterm Hypoxic-Ischemic Encephalopathy

Krishna Revanna Gopagondanahalli  1 , Jingang Li  2 , Michael C Fahey  3 , Rod W Hunt  4 , Graham Jenkin  5 , Suzanne L Miller  5 , Atul Malhotra  3
Affiliations
Review

Preterm Hypoxic-Ischemic Encephalopathy

Krishna Revanna Gopagondanahalli et al. Front Pediatr. .

Abstract

Hypoxic-ischemic encephalopathy (HIE) is a recognizable and defined clinical syndrome in term infants that results from a severe or prolonged hypoxic-ischemic episode before or during birth. However, in the preterm infant, defining hypoxic-ischemic injury (HII), its clinical course, monitoring, and outcomes remains complex. Few studies examine preterm HIE, and these are heterogeneous, with variable inclusion criteria and outcomes reported. We examine the available evidence that implies that the incidence of hypoxic-ischemic insult in preterm infants is probably higher than recognized and follows a more complex clinical course, with higher rates of adverse neurological outcomes, compared to term infants. This review aims to elucidate the causes and consequences of preterm hypoxia-ischemia, the subsequent clinical encephalopathy syndrome, diagnostic tools, and outcomes. Finally, we suggest a uniform definition for preterm HIE that may help in identifying infants most at risk of adverse outcomes and amenable to neuroprotective therapies.

Keywords: asphyxia; cerebral palsy; encephalopathy; excitotoxicity; preterm brain injury.

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Figures

Figure 1
Figure 1
Pathophysiological mechanisms involved in preterm hypoxic–ischemic encephalopathy. Cx, cortex; SCWM, subcortical white matter; PVWM, periventricular white matter; BG, basal ganglia; IC, internal capsule.
See this image and copyright information in PMC

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