Hypoxia and Acute Brain Insult

Abstract

In practice, when an anoxia-associated brain insult has been extensive, patients do not recover consciousness despite adequate cardiopulmonary resuscitation. The persistence of acute neurological symptoms and signs reflect a significant period of impaired substrate delivery, which may or may not be associated with a depression in cerebral perfusion. In some of these patients diffuse cortical and basal ganglia changes may be seen on cranial CT or magnetic resonance imaging 24–72 hours after the cerebral insult. Interestingly the severity of such cerebral edema that occurs and its time course and association with cerebrovascular and cerebrometabolic dysfunction is influenced by the events around the time of the insult. For example, hypoxia-induced cardiac arrest, as may be seen in the child with a respiratory illness, is more commonly associated with the development of marked post-resuscitation cerebral edema when compared with the post-resuscitation features of patients suffering primary cardiac arrest. Specific basal ganglia changes which relate to later movement disorders in survivors may also be seen more commonly in patients suffering prolonged hypoxia without cardiac arrest, or cardiac arrest associated with low cerebral blood flow, protracted hypothermia and lactic acidosis.