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I. DEFINITION

  1. Neonatal encephalopathy (NE) is a clinically defined syndrome of disturbed neurologic function in the earliest days of life in infants born ≥35 weeks’ gestation, demonstrated by an altered level of consciousness or seizures and frequently associated with depressed respiratory drive, hypotonia, and depressed or absent reflexes. NE may result from a metabolic disorder, infection, drug exposure, hypoxic ischemic encephalopathy (HIE), or neonatal stroke. NE is the preferred terminology to describe a depressed newborn from any cause at the time of birth.

  2. Perinatal asphyxia is a condition of impaired blood gas exchange that, if it persistent, leads to progressive hypoxemia and hypercapnia. HIE, which is a subset of NE, can result from perinatal asphyxia whereby inadequate oxygen delivery to the brain leads to compromised brain metabolism

  3. The likelihood that acute intrapartum or peripartum hypoxia-ischemia (HI) may have contributed to NE is based on the following factors identified by the American College of Obstetricians and Gynecologists (ACOG) task force on NE:

    1. Neonatal signs

      1. Apgar score <5 at 5 minutes and 10 minutes.

      2. Fetal umbilical artery acidemia pH <7 and base deficit >12 mmol/L or both.

      3. Neuroimaging evidence of acute brain injury seen on brain magnetic resonance imaging (MRI) or magnetic resonance spectroscopy consistent with HI.

      4. Presence of multisystem organ failure consistent with HIE.

    2. Type and timing of contributing factors

      1. A sentinel hypoxic or ischemic event occurring immediately before or during labor and delivery.

      2. Fetal heart rate monitor patterns consistent with an acute peripartum or intrapartum event.

      3. Timing and type of brain injury patterns based on imaging studies consistent with an etiology of an acute peripartum or intrapartum event.

      4. No evidence of other proximal or distal factors that could be contributing factors.

    3. Developmental outcome

      1. Developmental outcome is spastic quadriplegia or dyskinetic cerebral palsy. Other subtypes of cerebral palsy (CP) and other developmental abnormalities are not specific to acute intrapartum HIE.

II. INCIDENCE

NE occurs in 3.0 per 1000 live term births and leads to death in 15% to 20% of cases and permanent neurologic deficits in 25% of infants. It is estimated that 70% of cases of NE are due to events that arise before onset of labor, 20% are due to intrapartum events, and 10% are due to postnatal complications. Several case-control studies suggest that a combination of antepartum and intrapartum events is involved in moderate to severe NE. HIE has an incidence of 1.5 per 1000 live births. The worldwide prevalence of CP is 2 to 3 per 1000 live births. Intrapartum hypoxia-acidemia accounts for only approximately 10% to 20% of CP cases.

III. PATHOPHYSIOLOGY

  1. Hypoxic ischemic injury. A reduction in oxygen delivery precipitates an immediate drop in cellular high-energy phosphate levels, which is termed a primary energy failure. Lactic acid accumulation leads to cellular swelling via failure of membrane ion pump. Calcium influx releases glutamate and ultimately leads to an excitotoxic cycle resulting in free ...

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