Protecting the term newborn brain following hypoxia–ischaemia

Abstract

Following hypoxia–ischaemia, prompt resuscitation is required to re-establish oxygenation and perfusion. Thereafter, the clinical condition requires strict attention to detail. Ventilation may be required to ensure oxygenation; hyperventilation must be avoided. Myocardial dysfunction is common and inotropes may be required to support cerebral perfusion. Normoglycaemia should be maintained. Seizures further compromise neuronal viability and should be treated if frequent or prolonged. Initial fluid restriction is advised in anticipation of renal dysfunction, rather than prevention of cerebral oedema. Other causes of an acute neonatal encephalopathy need to be considered. Animal models of hypoxia–ischaemia indicate that neuronal injury continues beyond the termination of the initial insult. There have been a number of neuroprotective treatments developed from these models and they aim to interrupt the cascade leading to delayed neuronal death. Hypothermia as a strategy appears promising and is currently being evaluated by means of a number of randomized controlled clinical trials.