Is Periventricular Leucomalacia aResult of Hypoxic-Ischaemic Injury?

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Abstract
Decrease in the arterial partial pressure of carbon dioxide (PaCO2) causes a reduction in cerebral blood flow in humans and in most animal species; in adults as well as in newborns and even in fetal life. Severely decreased PaCO2 increases cerebral lactate production, modifies spontaneous electric brain activity, and may decrease the metabolic rate of oxygen. A relation between very low PaCO2 and brain injury, however, has not been shown in adult humans or full-term newborn infants, nor in perinatal animals. In contrast, an association between low PaCO2 and cerebral palsy and white matter injury in preterm infants has been reported repeatedly. A cause-and-effect relation is suggested by data from the immature rat: brain damage induced by ligation of a carotid artery can be reduced by adding CO2 to the inspired gas and hence avoiding the consequences of spontaneous hyperventilation. This may be relevant for the clinical care of preterm infants, since PaCO2 to a large extent is a function of respiratory management. The questions to be addressed are whether hypocapnia sensitises the brain to hypoxaemia, and also whether the escape mechanisms are less effective in the preterm human brain.