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.

Introduction

Ethical questions in medicine revolve around three core topics: what needs to be decided, on what basis, and by whom. These matters are not unique to the perinatal period, nor to patients with brain injury, but both of those circumstances may have ethical implications in the decision-making process, and in combination they raise questions that are unique. Because these situations touch so many critical aspects of human existence – birth, death, personhood, parenthood, etc. – it is not surprising that ethical matters related to the perinatal period have garnered a disproportionate amount of attention in the public discourses on medical ethics, nor that brain integrity lies at the core of so many of the contentious cases. The philosophical underpinnings of medical ethics have been reviewed exhaustively in many other venues, so this discussion will focus on aspects that are unique to or uniquely framed by brain injury or dysfunction in the perinatal period.

What is to be decided?

In the lay literature, ethical dilemmas are often framed as “life-or-death” decisions, with the implication that death or survival are options to be freely selected by patients, family members, or care providers, and that the ultimate outcome is within their control. In reality, that is rarely the case. In the case of a patient whose vital signs are rapidly failing despite full application of intensive care measures, this fact is obvious and there is no (or at most a very short-lived) ethical problem.

In preparing the fourth edition of our textbook, we have incorporated the newest data regarding the pathophysiology and cellular and molecular bases of neonatal encephalopathy. We have added the most recent data depicting the emergence of newer and promising forms of therapy, including the results of randomized clinical trials using hypothermia.

We have added two new editors for this edition, Dr. Maurice L. Druzin, who is the Chief of Maternal Fetal Medicine at Stanford University, and Susan R. Hintz, an Associate Professor of Pediatrics in the Division of Neonatal and Developmental Medicine. Dr. Druzin has reorganized the section on obstetrical factors that can contribute to fetal and neonatal brain injury and has recruited new contributors for this endeavor. Dr. Hintz, who has provided leadership in prenatal counseling and is the Director of our new Center for Comprehensive Fetal Health, has also focused on outcome studies in various disease processes in the neonate, and recruited new contributors to provide additional outcome data and recommendations.

We have added several new chapters, including ones addressing pregnancy-induced hypertension, HELLP syndrome and chronic hypertension, complications of multiple gestation, neurogenic disorders of the brain, pathogenesis of white-matter injury in the preterm infant, neonatal stroke, assessment and management of infants with cerebral palsy, the long-term outcome of neonatal events on speech, language development, and academic achievement, as well as the neurological outcome of infants with neonatal encephalopathy.

Introduction

After the initial resuscitation of an encephalopathic infant, the extended management of the patient becomes critical in order to prevent as much secondary damage as possible. There are many different management protocols that are acceptable, and it is not the intent of this chapter to review all of them used for the various conditions encountered in neonatal intensive care. Rather, we focus on the early transitional period following birth and resuscitation, during which the condition of the depressed infant can be substantially improved by expert care.

As noted in Chapters 2 and 42, the encephalopathic period involves a continuum of biologic events associated with secondary energy failure lasting up to 48–72 hours after the initial insult. These include the reperfusion period with the elaboration of oxygen free radicals and various cytokines as well as necrosis and apoptosis that then ensue. It is imperative that the extended management of these infants be carried out in an optimal fashion at a center that can provide hypothermia or other novel neuroprotective interventions that may be developed.

Unfortunately, the windows of opportunity may be short and variable depending upon the nature of the intervention, and could change as further research informs practice. Thus there is an obligation for the practitioner to be well informed about progress in the standard of care and to stay current with respect to neuroprotective strategies. Various neuroprotective mechanisms after hypoxic–ischemic injury are discussed in detail in Chapter 42.