Electronic fetal monitoring: The difficulty of linking patterns with outcomes
Nonreassuring tracings don’t always correlate with adverse outcomes, and vice versa. A look at what we know and don’t know from evidence to date.
Human factors
Agreement between observers. The reliability and reproducibility of EFM interpretation have been reviewed, but prospective studies to evaluate them are lacking. Interobserver agreement is reasonably high for the baseline rate, accelerations, and decelerations, but lower for variable decelerations and lower still for variability. Computers have been investigated for standardizing EFM interpretation.
Competency of physicians and nurses. A study14 assessing competency in the evaluation of EFM tracings surveyed 43 Ob/Gyn training programs.
Researchers found that the majority (79%) use clinical experience along with structured lectures (87%) to train residents and fellows. Perinatal morbidity and mortality conferences were used by 85% of programs, and maintenance of EFM skills involved both clinical experience and case studies.
Although registered nurses typically undergo annual competency evaluation in EFM, physician competency is not formally evaluated. Thus, some other mechanism for ensuring expertise would be helpful.
Unreliable link to outcomes
The correlation between FHR patterns and neonatal outcomes is difficult to establish. The causative event in 70% of neonatal encephalopathy cases is believed to have occurred before the onset of labor13; therefore, few cases of cerebral palsy and neonatal encephalopathy are amenable to interventions during labor. Abnormal patterns that do not allow sufficient time for intervention also may have poor outcomes.
Fetuses that have intrapartum asphyxia usually have abnormal heart rate patterns. However, most women with abnormal FHR patterns give birth to neonates with normal Apgar scores and outcomes.
The central tenet of the 2003 monograph13 by the American College of Obstetricians and Gynecologists is that in order for an intrapartum event to progress to cerebral palsy, the pathway must proceed through neonatal encephalopathy. However, only 30% of neonatal encephalopathy cases are due to events during labor. Further, epilepsy, mental retardation, and attention deficit disorder are not caused by birth asphyxia.
A 99% false-positive rate may result when nonreassuring EFM tracings are used to predict cerebral palsy. For this reason, there is still considerable disagreement about whether EFM can reduce the incidence of cerebral palsy. Using the criteria for establishing acute hypoxic-ischemic insult (TABLE 1) and for determining that intrapartum events were sufficient to cause cerebral palsy (TABLE 2), only 9% of cerebral palsy cases are attributable to possible birth asphyxia.11
Most cases of catastrophic hypoxia ultimately lead to fetal or neonatal death; a minority of infants survive and develop cerebral palsy. The pattern of neurologic injury following acute catastrophic hypoxic-ischemic insult can involve the basal ganglia and thalami; it may be different from the pattern that commonly follows chronic insult, which involves primarily the cerebral cortex and subcortical white matter.
TABLE 1
Criteria for establishing acute hypoxic-ischemic insult
| Metabolic acidosis evident in fetal umbilical cord arterial blood at delivery (pH <7.0 or base excess ≥ 12 mmol/L) |
| Early onset of severe or moderate neonatal encephalopathy in infants delivered at ≥ 34 weeks’ gestation |
| Cerebral palsy of the spastic quadriplegic or dyskinetic type |
| Exclusion of other identifiable causes |
| Data from American College of Obstetricians and Gynecologists13 |
TABLE 2
Criteria to establish intrapartum event as cause of cerebral palsy
| Sentinel hypoxic event occurring immediately before or during labor |
| Sudden sustained fetal bradycardia or absence of fetal heart rate variability in presence of persistent late or variable decelerations |
| Apgar score of less than 3 at 5 minutes |
| Onset of multisystem involvement within 72 hours of birth |
| Early imaging studies showing evidence of acute nonfocal abnormality. |
| Data from American College of Obstetricians and Gynecologists13 |
Little time to react during labor
Severe intrapartum hypoxic-ischemic insult may be detected by EFM but, in some cases, the reaction time to prevent fetal brain injury is very short. These intrapartum events include umbilical cord prolapse, shoulder dystocia, uterine rupture, and maternal cardiopulmonary arrest. With uterine rupture, asphyxia may occur as quickly as 10 minutes after onset of bradycardia when the prolonged deceleration is preceded by severe late decelerations of 30 to 90 minutes. The average time from onset of prolonged bradycardia has been reported as 13±6.5 minutes.13
The 30-minute rule. Because mortality and morbidity may depend on how much time elapses from onset of the catastrophic event to delivery, ACOG developed guidelines for timing emergent cesarean. The 30-minute rule13 advises that a cesarean be performed within 30 minutes of the decision to proceed. Unfortunately, in many cases, acute hypoxic-ischemic insult occurs in less than 30 minutes.
Many hospitals and obstetric services no longer offer vaginal birth after cesarean (VBAC) if they cannot guarantee that anesthesia, nursing, pediatric, and operating room services will be available within this time frame. However, other causes of sudden hypoxia—besides the small chance of uterine rupture with VBAC—may be neither predictable nor preventable.
