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    Updates on neonatal encephalopathy and cerebral palsy



    Dr. Lockwood, Editor-in-Chief, is Dean of the Morsani College of Medicine and Senior Vice President of USF Health, University of South Florida, Tampa. He can be reached at [email protected] 


    To get a sense of the magnitude of the medicolegal threat and economic drain posed by the plaintiff’s bar from cerebral palsy (CP) lawsuits, just google “cerebral palsy lawsuits.” You will be astonished by the misinformation and recklessness contained in many of the 350,000-plus sites that come up. Into this sea of misinformation sails the second edition of ACOG’s Neonatal Encephalopathy and Neurologic Outcome.1

    ACOG’s Task Force on Neonatal Encephalopathy was commissioned by President Richard Waldman, MD, and chaired by Mary D’Alton, MD. At more than 230 pages, the report is not for the faint of heart, but it is crammed with the latest findings on the etiology, diagnosis, prevention, and treatment of neonatal encephalopathy (NNE) and CP.

    I encourage all ob/gyns to read it carefully, and it is a must-read for department chairs, residency program directors, and those involved in hospital patient safety efforts.


    First, definitions: NNE is defined as the clinical syndrome of “disturbed neurological function in the earliest days of life in an infant born at or beyond 35 weeks of gestation, manifested by a subnormal level of consciousness or seizures and often accompanied by difficulty with initiating and maintaining respiration and depression of tone and reflexes.”1

    CP describes a cluster of disorders manifest by nonprogressive motor disabilities (spasticity, dyskinesis, and ataxia) that can occur to infants born at any gestational age. Not all cases of NNE result in CP and not all cases of CP are associated with prodromal NNE. The risk of CP increases with earlier gestational ages at delivery, with very preterm delivery (<32 weeks’ gestation) being the single-greatest risk factor. Hypoxic-ischemic encephalopathy (HIE) is but one of many causes of both NNE and CP. Neonatal encephalopathy complicates 2.7 to 3.3 per 1000 live births, CP 2 to 2.5/1000 live births, and HIE 1.3 to 1.7/1000 live births.1 The rates of CP among term infants have remained remarkably stable over time at 1.4 to 1.8 per 1000, despite a significantly increased cesarean delivery rate.1 The occurrence of CP without antecedent NNE excludes HIE as a cause.

    Prior epidemiologic studies suggested that 69% of NNE cases were the result of factors occurring prior to the onset of labor, whereas only 29% were associated with intrapartum events and only 5% could be exclusively linked to intrapartum factors.2 Major risk factors for NNE include preterm and postterm birth, fetal growth restriction, preeclampsia, perinatal infections, chorioamnionitis, maternal thyroid disease, placental abnormalities, infertility treatment with resultant multiple gestations, and prematurity.


    Charles J. Lockwood, MD, MHCM
    Dr. Lockwood, Editor-in-Chief, is Dean of the Morsani College of Medicine and Senior Vice President of USF Health, University of South ...


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