Is periventricular leucomalacia a result of hypoxic-ischaemic injury? Hypocapnia and the preterm brain

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, anassociation 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 pre-term human brain.