An integrated model for haemorrhagic and ischaemic lesions in the newborn brain.

Abstract

The vascular anatomy of the developing brain changes from a predominantly basal ganglia orientated pattern at 24 wk to a cortically orientated pattern by 34 wk. This information, combined with other known data on cerebral vascular anatomy and physiology, allows us to develop a model for haemorrhagic and ischaemic lesions in the newborn brain based on two main series of reactions. One series involves the effects of hypoxia and hypercapnia in leading to breakdown of the blood--brain barrier with resultant oedema or haemorrhage. The other links a fall in perfusion pressure and factors causing vasoconstriction with the development of ischaemic lesions. Application of the model involves additional consideration of the state of development of the cerebral vessels at the gestational age concerned. The model helps to explain the observed findings in germinal layer haemorrhage/intraventricular haemorrhage, periventricular leukomalacia and venous infarction, in the preterm brain. Its use also suggests that there are three patterns of vulnerability in the term infant brain. The model carries several implications for the neonatal management of preterm infants. Routine continuous monitoring of blood pressure is of critical importance as cerebral blood flow may vary with blood pressure in the ill newborn. It is important to avoid head compression which may lead to impaired cerebral perfusion. Finally, control of the acid--base status is essential for maintenance of the blood--brain barrier. Correction of abnormal values must be carried out without provoking rapid swings in either the serum osmolarity or the blood pressure.