hey add the caveat that no one strategy is infallible, and thus, no single strategy will achieve 100-percent certainty in attributing a cause to neonatal encephalopathy.
he 20 14 Task Force defined neonatal encephalopathy as a syndrome of neurological dysfunction identiied in the earliest days of life in neonates born at :35 weeks' gestation. It is manifested by subnormal levels of consciousness or seizures and oten accompanied by diiculty with initiating and maintaining respiration and by depressed tone and relexes. he incidence of encephalopathy has been cited to be 0.27 to 1.1 per 1000 term liveborn neonates, and it is much more frequent in preterm newborns (Ensing, 2013; Plevani, 2013; Takenouchi, 2012; Wu, 2011). Although the 2014 Task Force concluded that there are many causes of encephalopathy and cerebral palsy, it focused on HIE and those that were thought to be incurred intrapartum. To identiy afected infants, a thorough evaluation is necessary and includes maternal history, obstetrical antecedents, intrapartum factors, placental pathology, and newborn course. hese are complemented by laboratory and neuroimaging indings.
There are three clinically deined levels. Mild encephalopathy is characterized by hyperalertness, irritability, jitteriness, and hypertonia and hypotonia. Moderate encephalopathy is manifest by lethargy, severe hypertonia, and occasional seizures. Severe encephalopathy is manifest by coma, multiple seizures, and recurrent apnea.
The 20 14 Task Force also concluded that of the several forms of cerebral palsy, only the spastic quadriplegic type can result from acute peripartum ischemia. Other forms-hemiparetic or hemiplegic cerebral palsy, spastic diplegia, and ataxia-are unlikely to result from an intrapartum event. Purely dyskinetic or ataxic cerebral palsy, especially when accompanied by a learning disorder, usually has a genetic origin (Nelson, 1998).
he 2014 Task Force radically revised its 2003 criteria used to deine an acute peripartum event that is consistent with an HIE and neonatal encephalopathy. hese are outlined in Table 33-1 and are considered with the following caveats.
TABLE 33-1 . Findings Consistent with an Acute Peripartum or Intrapartum Event Leading to Hypoxic-Ischemic Encephalopathy
Apgar score: <5 at 5 and 10 minutes
Umbilical arterial acidemia: pH <7.0 and/or base deficit :12 mmol/L
Neuroimaging evidence of acute brain injury: MR imaging or MRS consistent with HIE Multisystem involvement consistent with HIE
Type and Timing of Contributing Factors
Fetal heart rate monitor patterns consistent with an acute peripartum or intrapartum event
HIE = hypoxic ischemic encephalopathy; MR = magnetic resonance; MRS = magnetic resonance spectroscopy.
Summarized from the American College of Obstetricians and Gynecologists, 2014b.
First, Apgar Scores that are low at 5 and 10 minutes are associated with greater risk for neurological impairment. Low scores stem from many causes, and most of these infants will not develop cerebral palsy. With a 5-minute Apgarr? 7, it is unlikely that peripartum HIE caused cerebral palsy.