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HIGH-RISK OBSTETRICS SERIES: AN EXPERT'S VIEW |
From the Division of Maternal–Fetal Medicine, Department of Obstetrics and Gynecology, The University of Texas Medical Branch, Galveston; and Section of Neonatology, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.
Address reprint requests to: Gary D. V. Hankins, MD, The University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0587; E-mail: ghankins{at}utmb.edu.
The topics of neonatal encephalopathy and cerebral palsy, as well as hypoxic–ischemic encephalopathy, are of paramount importance to anyone who ventures to deliver infants. Criteria sufficient to define an acute intrapartum hypoxic event as sufficient to cause cerebral palsy have been advanced previously by both The American College of Obstetricians and Gynecologists (ACOG) and the International Cerebral Palsy Task Force. ACOG convened a task force that over the past 3 years reviewed these criteria based upon advances in scientific knowledge. In this review, we cover the slow but steady progression toward defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy. Four essential criteria are also advanced as prerequisites if one is to propose that an intrapartum hypoxic–ischemic insult has caused a moderate to severe neonatal encephalopathy that subsequently results in cerebral palsy. Importantly, all four criteria must be met: 1) evidence of metabolic acidosis in fetal umbilical cord arterial blood obtained at delivery (pH less than 7 and base deficit of 12 mmol/L or more), 2) early onset of severe or moderate neonatal encephalopathy in infants born at 34 or more weeks’ gestation, 3) cerebral palsy of the spastic quadriplegic or dyskinetic type, and 4) exclusion of other identifiable etiologies, such as trauma, coagulation disorders, infectious conditions, or genetic disorders. Other criteria that together suggest intrapartum timing are also discussed.
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