Perinatal asphyxia or hypoxic ischemic encephalopathy (HIE) is a condition of impaired blood gas exchange during the intrapartum period that, if it persists, leads to progressive hypoxemia and hypercapnia with a metabolic acidosis. HIE is a subset of neonatal encephalopathy (NE).
Neonatal encephalopathy (NE) is clinically defined as a disturbance in neurologic function demonstrated by difficulty in maintaining respirations, hypotonia, altered level of consciousness, reflexes, seizures, and poor feeding. NE does not imply HIE. NE may represent a metabolic disorder, infection, drug exposure, or neonatal stroke and is the preferred terminology to describe a depressed newborn at the time of birth.
Definition of perinatal asphyxia
The definition of perinatal asphyxia is imprecise. Essential criteria required to define an acute intrapartum event include:
Evidence of a metabolic acidosis in fetal umbilical cord arterial blood obtained at delivery (pH <7.00 and base deficit ≥12 mmol/L).
Early onset of severe or moderate neonatal encephalopathy in infants born at ≥34 weeks' gestation.
Exclusion of other identifiable etiologies such as trauma, coagulation disorders, infections, or genetic disorders.
Criteria that collectively suggest an intrapartum event, but individually do not, include:
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.
Apgar scores of 0–3 >5 min of life.
Onset of multiorgan involvement within the first 3 days of life.
Early imaging study showing evidence of acute nonfocal cerebral abnormality.
Biochemical indices. There is no specific blood test to diagnose perinatal asphyxia.
Fetal acidemia. Neonatal morbidity increases as umbilical arterial pH falls below 7.0. The metabolic component (base deficit and bicarbonate) is more important than the respiratory component (PCO2). Isolated respiratory acidosis is not typically associated with neonatal complications. The precise value that is required to define damaging acidemia is not known. A pH <7.0 realistically represents clinically significant acidosis. Acidemia alone does not establish that hypoxic injury has occurred.
Umbilical artery PO2 levels are not predictive of adverse neonatal outcome.
It is a poor tool for assessing asphyxia. Low Apgar scores are unlikely to be the cause of morbidity but rather the results of prior causes.
An infant with an Apgar score of 0–3 at 5 min, improving to ≥4 by 10 min, has >99% chance of not having cerebral palsy (CP) at 7 years of age; 75% of children who develop CP have normal Apgar scores at birth.
A 1996 revised American Academy of Pediatrics/American College of Gynecologists and Obstetricians statement emphasized that the Apgar score alone should not be used as evidence that neurologic damage was caused by hypoxia resulting in neurologic injury or by inappropriate intrapartum management.
Incidence. The incidence of HIE is 2–9 in 1000 live term births. The incidence of CP has not fallen despite improved obstetric and neonatal interventions and remains at 1–2 in 1000 live term births. 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. One cannot state with a reasonable degree ...
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