++
Perinatal asphyxia is a condition of impaired blood gas exchange that, if persistent, leads to progressive hypoxemia and hypercapnia. Hypoxic-ischemic encephalopathy (HIE), which is a subset of neonatal encephalopathy (NE), can result from perinatal asphyxia.
Neonatal encephalopathy (NE) is clinically defined as a disturbance in neurologic function demonstrated by difficulty in maintaining respirations, hypotonia, altered level of consciousness, depressed or absent primitive reflexes, seizures, and poor feeding. NE does not imply HIE. NE may represent a metabolic disorder, infection, drug exposure, or neonatal stroke, but it is the preferred terminology to describe a depressed newborn from any cause at the time of birth.
In order for an acute intrapartum hypoxic event to be considered a cause of cerebral palsy (CP), the American Academy of Pediatrics (AAP) and the American College of Obstetrics and Gynecology (ACOG) define 4 essential criteria that must be met:
Evidence of a metabolic acidosis in fetal umbilical cord arterial blood obtained at delivery (pH <7 and base deficit ≥12 mmol/L).
Early onset of severe or moderate neonatal encephalopathy in infants born at 34 or more weeks of gestation.
CP of the spastic quadriplegic or dyskinetic type.
Exclusion of other identifiable etiologies, such as trauma, coagulation disorders, infectious conditions, or genetic disorders.
Criteria that collectively suggest an acute intrapartum hypoxic event (within 0–48 hours to labor and delivery) but are individually nonspecific to asphyxial insults:
A sentinel hypoxic event occurring immediately before or during labor
A sudden and sustained fetal bradycardia or the absence of fetal heart rate variability in the presence of persistent, late, or variable decelerations, usually after a hypoxic sentinel event when the pattern was previously normal
Apgar scores of 0–3 beyond 5 minutes
Onset of multisystem involvement within 72 hours of birth
Early imaging showing evidence of acute nonfocal cerebral abnormality
++
Data regarding perinatal asphyxia rates from 2001 indicate a prevalence rate of 25 per 1000 term live births and 73 per 1000 preterm live births, with 15 and 50% moderate to severe cases, respectively. The overall incidence of NE attributable to perinatal asphyxia was ∼1.6 per 10,000 live births in the absence of preconception or antepartum abnormalities. European data indicate an overall CP rate of 2.08 per 1000 live births for the period 1980–1990, with increased rates seen in infants with birthweight <1500 g. While earlier studies showed a stable rate of CP between the 1950s and 1990s, more recent data indicate a decline in the prevalence of CP for preterm infants born after 1980, possibly reflecting improved perinatal care. Only 8–17% of CP in term infants is associated with adverse perinatal events suggestive of asphyxia; the cause of ≥90% of cases remains unknown.
++
Hypoxic-ischemic injury. The asphyxial event results in cerebral ischemia, which precipitates an immediate drop in cellular high-energy phosphate levels, termed primary energy failure. Glutamate, an excitatory amino acid, is also released in substantial amounts due to cellular depolarization. N-methyl-d-aspartate (NMDA) receptors are subsequently overstimulated by glutamate and result in increased intracellular calcium and necrotic cell death. Cerebral blood flow is restored in the reperfusion period with normalization of cellular energy levels within 2–3 hours after the insult. A latent phase follows and lasts 6–15 hours, during which oxidative metabolism returns to baseline, but secondary inflammation and ...