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Chapter 24: Neonatal Resuscitation: Pathophysiology, Organization, and Survival

Keith S. Meredith; Pranav Patel

INTRODUCTION

Each year, an estimated 23% of the 3.5 million neonatal deaths that occur worldwide are the result of birth asphyxia. In the United States, preliminary 3.9 million children are born annually, with a reported infant mortality rate of 6.11 for the year 2011.1,2 This suggests that every year, among US children who reach 28 weeks’ gestation, over 26,000 die prior to their seventh day of life. A significant portion of those infants who succumb do so from birth asphyxia. Further, among children reaching term gestation, 2 to 3 per 1000 live term births suffer hypoxic ischemic encephalopathy (HIE), (0.3 per 1000 severe HIE). (Table 24-1) Up to 80% of infants who survive severe hypoxic-ischemic encephalopathy develop serious complications and 10% to 20% develop moderately serious disabilities. In addition, it is widely accepted that 10% of all newborns require some assistance to begin and maintain normal breathing and that 1% require aggressive resuscitation. Thus, using the national birth rate data, annually 400,000 newborns need some help during the perinatal period, 40,000 per year require expert assistance to reverse profound cardiorespiratory depression, and 1200 per year develop severe HIE. Although there is some evidence that therapeutic hypothermia is beneficial to term newborns with moderate to severe hypoxic ischemic encephalopathy, and that cooling decreases death without increasing major disability in survivors, this therapy is not available at all centers yet as further research is being compiled. (Table 24-2).

TABLE 24-1.ACOG and American Academy of Pediatrics (AAP) Task Force on Neonatal Encephalopathy and Cerebral Palsy
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TABLE 24-1. ACOG and American Academy of Pediatrics (AAP) Task Force on Neonatal Encephalopathy and Cerebral Palsy

Part 1 Four essential criteria (all 4 must be met)

  • Evidence of metabolic acidosis in fetal umbilical cord arterial blood obtained at delivery (pH <7 and base deficit of ≥12 mmol/L)

  • Early onset of severe or moderate neonatal encephalopathy in infants born at 34 or more wks of gestation

  • Cerebral palsy of the spastic quadriplegic or dyskinetic type

  • Exclusion of other identifiable etiologies, such as trauma, coagulation disorders, infectious conditions, or genetic disorders

Part 2 Criteria that may suggest intrapartum timing, but nonspecific for an asphyxial insult

  • A sentinel (signal) hypoxic event occurring immediately before or during labor. A serious pathologic event has to occur for a neurologically intact fetus to sustain a neurologically damaging acute insult

  • A sudden and sustained fetal bradycardia or the absence of fetal heart rate variability in the presence of persistent late or persistent variable decelerations, usually after a hypoxic sentinel event when the pattern was previously normal

  • Apgar scores of 0-3 beyond 5 min

  • Onset of multisystem involvement within 72 h of birth

  • Early imaging study showing evidence of acute nonfocal cerebral abnormality

Data from http://www.acog.org/from_home/Misc/neonatalEncephalopathy.cfm?printerFriendly=yes

TABLE 24-2.Criteria for Hypothermia Therapy
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TABLE 24-2....

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