Abstract
Neonatal hypoxic–ischaemic brain damage is a leading cause of child mortality and morbidity, including cerebral palsy, epilepsy, and cognitive disabilities. The majority of neonatal hypoxic–ischaemic cases arise as a result of impaired cerebral perfusion to the foetus attributed to uterine, placental, or umbilical cord compromise prior to or during delivery. Bacterial infection is a factor contributing to the damage and is recorded in more than half of preterm births. Exposure to infection exacerbates neuronal hypoxic–ischaemic damage thus leading to a phenomenon called infection-sensitised hypoxic–ischaemic brain injury. Models of neonatal hypoxia–ischaemia (HI) have been developed in different animals. Both human and animal studies show that the developmental stage and the severity of the HI insult affect the selective regional vulnerability of the brain to damage, as well as the subsequent clinical manifestations. Therapeutic hypothermia (TH) is the only clinically approved treatment for neonatal HI. However, the number of HI infants needed to treat with TH for one to be saved from death or disability at age of 18–22 months, is approximately 6–7, which highlights the need for additional or alternative treatments to replace TH or increase its efficiency. In this review we discuss the mechanisms of HI injury to the immature brain and the new experimental treatments studied for neonatal HI and infection-sensitised neonatal HI.
Highlights
The interruption of blood and oxygen supply to the foetal brain during pregnancy and at the time of birth is a leading cause of neonatal hypoxic–ischaemic (HI) brain damage
The majority of cell death occurs via necrosis, apoptosis [caspase 3 dependent, Bcl-2-associated X protein (Bax)/B-cell lymphoma 2 (Bcl-2) pathway], autophagy, and apoptosis–necrosis continuum leading to cellular atrophy (Peng and Greenamyre, 1998; Puka-Sundvall et al, 2000; Johnston et al, 2002; Northington et al, 2007)
This review aims to provide an update on the new proposed treatments which are studied for neonatal HI and infectionsensitised HI
Summary
The interruption of blood and oxygen supply to the foetal brain during pregnancy and at the time of birth is a leading cause of neonatal hypoxic–ischaemic (HI) brain damage. Known as neonatal hypoxic–ischaemic encephalopathy (HIE), this condition affects 1–3 per 1000 live births in developed countries, increasing to 26 per 1000 in the developing world (Rocha-Ferreira and Hristova, 2016). Despite the advantages in neonatal health care, a quarter of all neonatal deaths is due to HIE (Lawn et al, 2005; Rocha-Ferreira and Hristova, 2016), and 30% of the sufferers of neonatal HI brain damage develop disabilities, including cerebral palsy, seizures, and cognitive and memory impairment (Rocha-Ferreira and Hristova, 2016; Lundgren et al, 2018).
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