Introduction

Since the publication of the first edition of this text in 1989, a great deal has been written regarding the issues of neonatal asphyxia and hypoxic–ischemic encephalopathy (HIE) in term and near-term infants. These manuscripts have addressed the incidence, etiology, pathophysiology, treatment, and outcome of such patients, often relating outcomes to the development of cerebral palsy (CP) and/or mental retardation in survivors. Much of the understanding of the pathophysiology has been the result of studies carried out in laboratory animals, which have been extrapolated to the human fetus and newborn. Additional studies of complications and outcome have been population-based, comparing the injured infant to carefully selected normal controls. These studies have added a great deal to our understanding of risk factors for brain injury, and have enhanced our ability to predict and to identify patients with increasing accuracy. This has become increasingly important, as newer modalities of treatment have evolved which require more precision in the early identification of these infants so that the validity of these therapies can be ascertained. As can be seen in Chapters 39, 41, and 42, early institution of treatment becomes of paramount importance if an improved outcome is to be achieved.

While some still believe that the major injuries in these patients occur in the intrapartum period, many studies suggest otherwise, and allude to the fact that many of the problems arise antenatally, and may be exacerbated in the intrapartum period.

Introduction

Following the birth of a depressed newborn, the infant's caretakers are involved in providing appropriate resuscitative techniques, stabilizing the infant's biochemical and physiological abnormalities, and evaluating the infant's response to these measures. The caretakers must also ascertain the cause of the infant's depression, attempt to determine when the event or events leading to the depression occurred, and develop a plan for follow-up evaluation and treatment that will be required. The determination of causation and timing not only has medical–legal implications, but also is becoming extremely important in order to evaluate the types of therapy that may be utilized to mitigate the effects of an asphyxial event. If the infant had suffered significant damage days or weeks prior to birth, then these rescue forms of therapy will have little, if any, beneficial effect on the infant's eventual outcome. In many situations, this determination is very difficult to make, as there may be a myriad of events that could have occurred prior to the time of birth, and overlapping of significant problems makes this exercise an almost impossible task at times.

Identification of the etiology of a cerebral injury is a critical prerequisite to the determination of its timing. For example, lactic acidemia immediately after birth and an elevated serum creatine kinase (CK) level at 24 hours of age in an infant with abnormal intensities of T1- and T2-weighted signals in the basal ganglia on MRI obtained at 2 weeks of age might point to intrapartum timing of an acute hypoxic–ischemic insult.