The postnatal management of the asphyxiated term infant.

Investigations in animal models of hypoxic-ischemic injury have not translated into clinical trials of success because of the complex pathology of hypoxic-ischemic brain injury in neonates, the difficulty in defining the onset and duration and severity of the injury, the underlying predisposing disorders of the mothers or the infant, the side effects of many of the investigational drugs precluded clinical use, and many of the investigational agents interfered with only one step of the cascade of events that lead to brain injury. It is possible that a combination of therapeutic agents, including those that affect different levels of the cascade to cell death, will have the greatest neuroprotective effects. Modest hypothermia postpones secondary energy failure and can prolong the window while pharmacotherapeutic agents can be used. It is possible that in the future, sequential administration of agents or strategies that are initiated in the intrapartum period and continued postnatally will be the optimum method for treating infants who are at highest risk for brain injury following acute hypoxic-ischemic asphyxia.