The Clinical Value of Intensive Monitoring in Term Asphyxiated Newborns

Perinatal asphyxia is an important cause of brain injury. It may lead to hypoxic-ischaemic encephalopathy (HIE) which occurs in one to six of every 1000 full term births. The risk of death or severe handicap is 0.5-2.0 out of 1000. Following intrapartum asphyxia cerebral hypoperfusion in combination with hypoxia produces characteristic neuropathological changes and related clinical signs. After the primary insult there is a thirty minutes period of reperfusion characterized by the partial recovery of cell and metabolic processes. This is followed by a latent phase which may last up to six hours. In this phase oxidative metabolism (near) normalizes (shown by MRspectroscopy) but EEG activity is depressed and the blood flow is likely to be reduced. Secondary energy failure and secondary hyperperfusion (‘luxury perfusion’) may occur in the neonatal brain within 6-15 hours after an acute ischaemic insult, marked by the acute onset of seizures (peaking at about 12 hours post insult). Excitotoxins accumulate in the cell and cell death may take 72 hours to completion. The infant’s gestational age and thus the maturational stage of the brain, as well as type, severity and duration of the insult are determinants of the brain injury. During the insult there is redistribution of blood flow to the brain, heart and adrenals. Our current understanding of perinatal asphyxia is based on animal experiments. Different and mixed etiologies lead to a range of post asphyxial patterns, usually subdivided into different patterns; acute, chronic or a combination of these two. With chronic, possibly repetitive insults, lesions are predominantly seen in (sub)cortical structures. This has been named watershed injury for its classical distribution along the borderzones between the major pial arteries, sparing thalamus and basal ganglia. From the literature it appears that watershed injury is observed most frequently in context of term birth asphyxia. In acute and (near) total asphyxia the damage is mostly to the thalami, basal ganglia, hippocampus, cerebellum, brain stem and specific areas of the neocortex like the rolandic, calcarine and insular cortex.