Neonatal Encephalopathy and Cerebral Palsy

“Neonatal Encephalopathy and Cerebral Palsy: Defining the Pathogenesis and Pathophysiology” was published in 2003 by the American College of Obstetricians and Gynecologists (ACOG) and the American Academy of Pediatrics (AAP). This report significantly broadened our understanding of the problem and provided the necessary information for evaluating the newborn with encephalopathy. An executive summary of the report entitled “Neonatal Encephalopathy and Cerebral Palsy: Executive Summary” (Obstetrics and Gynecology, 2004 103:780–81) is a useful reference.

Dr. R. Gibbs, et al., at the University of Colorado felt that applying the evidence contained in this report had great implications for risk management; however, the report did not make specific recommendations for clinical practice. Therefore, Dr. Gibbs, et al., wrote “Suggestions for Practice to Accompany Neonatal Encephalopathy and Cerebral Palsy” (Obstetrics and Gynecology, 2004 103:778–79). Both articles are available on the ACOG Web site (www.acog.org).

As noted in the forward of “Neonatal Encephalopathy and Cerebral Palsy,” “Until recently, four nonspecific clinical signs: 1) meconium-stained liquor, 2) non-reassuring fetal heart rate patterns, 3) low Apgar scores, and 4) neonatal encephalopathy were often assumed to be adequate evidence of birth asphyxia and hypoxic-ischemic neonatal encephalopathy in the absence of objective criteria to show that a de novo acute hypoxic event actually occurred during labor and delivery.” In reality, these four nonspecific signs often are the results of pathological insults to the newborn that occurred before labor and delivery.

These “Criteria to Define an Acute Intrapartum Hypoxic Event as Sufficient to Cause Cerebral Palsy” were developed by Drs. Henry Galan and Ronald Gibbs at the University of Colorado. It summarizes the “Suggestions for Practice” and provides a practical guideline to follow when faced with this difficult problem. Documenting the presence or absence of the 4 Essential and 5 Suggestive Criteria should be done in all cases of potential neonatal encephalopathy and cerebral palsy.

Please consider:

• Sharing this information with your entire perinatal “team,” e.g., Pediatrics, NICU, Anesthesia, L&D Personnel, etc.
• Developing written guidelines and protocols to apply the 12 “Suggestions for Practice” in your institution.
• Developing an interdisciplinary nomenclature at your institution that avoids nonspecific terms such as fetal distress and birth asphyxia.
  
  

Note: The yellow laminated copy of the “Criteria to Define an Acute Intrapartum Hypoxic Event as Sufficient to Cause Cerebral Palsy” sent by The Doctors Company to our insured physicians who provide obstetrical care contains an error. The error is in the 4 Essential Criteria. Criterion 2 should read “Early onset moderate or severe NNE (≥ 34 [not 24] weeks gestation).”

—David B. Troxel, M.D., Medical Director

Criteria to Define an Acute Intrapartum Hypoxic Event as Sufficient to Cause Cerebral Palsy

(NNE & CP-Defining Pathogenesis and Pathophysiology; ACOG & AAP; 2003)

4 Essential Criteria

1. Evidence of metabolic acidosis
   (pH<7.00; BD>12mmol/L)
2. Early onset moderate or severe NNE
   (≥ 34 weeks gestation)
3. CP of the spastic quadriplegic or dyskinetic type
4. Exclusion of other identifiable etiologies (trauma; coagulation disorders, infections, and genetic disorders)

5 Suggestive Criteria

1. A sentinel event (i.e., abruptio placenta, cord prolapse)
2. Sudden/sustained bradycardia w/o variability & w/ persistent late or variable decelerations
3. Apgar scores of 0-3 beyond 5 minutes
4. Onset of multisystem organ involvement within 72 hours
5. Early imaging study with evidence of acute nonfocal cerebral abnormality (MRI is optimal)

Suggestions for Practice to Accompany Neonatal Encephalopathy and Cerebral Palsy

(Obstetrics and Gynecology, 2004 103:778–79)

1. Based upon the ACOG monograph, neonatal encephalopathy (NNE) or cerebral palsy (CP) should not be attributed to an intrapartum event in a patient’s chart unless all four essential criteria are met.
2. Accordingly, after delivery of a newborn with risk factors for NNE, obtaining an umbilical artery pH and base deficit may help determine the timing of the insult. Such risk factors may include an infant with low Apgar scores, severe IUGR, non-reassuring heart rate tracings, a sentinel event, possibly thick meconium, etc.
3. A clamped segment of cord is stable for pH and blood gas assessment for at least 60 minutes, and a cord blood sample in a syringe flushed with heparin is stable up to 60 minutes. Umbilical artery blood is the basis for fetal acidosis. Umbilical vein blood may be helpful such as when there is a uteroplacental problem (i.e., abruption, maternal asthma, etc.).
4. For uncomplicated pregnancies with normal labor and delivery, with a normal vigorous infant, with normal Apgar scores at 1 and 5 minutes, the likelihood of severe metabolic acidosis and of NNE/CP due to an intrapartum event is so remote that routinely sending umbilical cord blood for pH and base deficit is not needed.
5. After delivery of an infant with risk factors for NNE, a detailed note should address as many of the 4 essential and 5 suggestive criteria as possible (i.e., OB note should include cord gas values, sentinel events, antepartum info, FHR pattern & Apgars; PEDS note should include OB notes + neurologic exam, organ dysfunction, relevant exclusion evaluations, and imaging, if done).
6. The term “perinatal asphyxia” should not be based upon meconium-stained AF, low Apgars, or non-reassuring FHR patterns as these are nonspecific markers.
7. In maternal & neonatal charts, avoid the term “fetal distress.” Use “non-reassuring FHR pattern” and document frequency, intensity, and duration of the FHR abnormality.
8. Gross and microscopic placental examination for causes other than hypoxia that may have predated labor. Key examples (not inclusive): maternal fever, chorioamnionitis, abruption, hypertension, meconium, cord abnormalities, stillbirth, neurologic problems, multiple gestation, IUGR, acidotic newborn, low Apgar scores, etc.).
9. In cases of NNE, a thorough investigation of causes should be carried out including a detailed family history, a detailed maternal history, placental examination, and, if appropriate, assessment of maternal or fetal thrombophilias, family genetic or metabolic conditions, cerebral or cerebrovascular anomalies, etc.
10. In the rare occurrence of CP, the type of CP should be carefully documented by a pediatric neurologist.
11. All fetal heart rate tracings should be labeled and archived.
12. With operative vaginal delivery, it is unclear whether the increased risk for NNE is due to the indication or the procedure itself. As such, notes should detail instrument used, application ease, procedure duration, pulls, pop-offs, attendants, etc.

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