Monitoring fetal electrocortical activity during labour for predicting worsening acidemia: a prospective study in the ovine fetus near term

Abstract

Background: Severe fetal acidemia during labour with arterial pH below 7.00 is associated with increased risk of hypoxic-ischemic brain injury. Electronic fetal heart rate (FHR) monitoring, the mainstay of intrapartum surveillance, has poor specificity for detecting fetal acidemia. We studied brain electrical activity measured with electrocorticogram (ECOG) in the near term ovine fetus subjected to repetitive umbilical cord occlusions (UCO) inducing FHR decelerations, as might be seen in human labour, to delineate the time-course for ECOG changes with worsening acidemia and thereby assess the potential clinical utility of fetal ECOG.

Methodology/principal findings: Ten chronically catheterized fetal sheep were studied through a series of mild, moderate and severe UCO until the arterial pH was below 7.00. At a pH of 7.24 ± 0.04, 52 ± 13 min prior to the pH dropping <7.00, spectral edge frequency (SEF) increased to 23 ± 2 Hz from 3 ± 1 Hz during each FHR deceleration (p<0.001) and was correlated to decreases in FHR and in fetal arterial blood pressure during each FHR deceleration (p<0.001).

Conclusions/significance: The UCO-related changes in ECOG occurred in advance of the pH decreasing below 7.00. These ECOG changes may be a protective mechanism suppressing non-essential energy needs when oxygen supply to the fetal brain is decreased acutely. By detecting such "adaptive brain shutdown," the need for delivery in high risk pregnant patients may be more accurately predicted than with FHR monitoring alone. Therefore, monitoring fetal electroencephalogram (EEG, the human equivalent of ECOG) during human labour may be a useful adjunct to FHR monitoring.

Conflict of interest statement

Competing Interests: The authors have read the journal's policy and have the following conflicts: Financial: Dr. Martin Frasch and Dr. Bryan Richardson are inventors of related patent applications entitled “EEG Monitor of Fetal Health” including U.S. Patent Application Serial No. 12/532,874 and CA 2681926 National Stage Entries of PCT/CA08/00580 filed March 28, 2008, with priority to US provisional patent application 60/908,587, filed March 28, 2007. The inventors have assigned their interests in the patent applications to the Lawson Health Research Institute who is the sole owner responsible for commercialization. The inventors are entitled to 50% of any net future revenue from commercialization after patenting and commercialization costs are deducted. Lawson Health Research Institute in all cases will retain rights to the academic and non-commercial use of the technology described in the related patent applications, which therefore does not alter the authors' adherence to all the PLoS ONE policies on sharing data and materials as detailed in the guide for authors.

Figures

Figure 1. Representative segments of fetal heart rate (BPM, beats per minute) and electrocorticogram (ECOG).

Umbilical cord occlusion (UCO) induced changes are shown in 15 minutes segments of FHR, ECOG amplitude (µV) and 95% spectral edge frequency (SEF, Hz). Baseline and the 1st hour of recovery are shown for comparison. Note an early emergence of the time correlated changes in FHR decelerations and increases in ECOG SEF with modest fetal acidemia (pH = 7.26). The arrows indicate fetal blood sampling and the corresponding pH values at these time points.

Figure 2. Representative segments of correlated changes in fetal heart rate decelerations (BPM, beats per minute) and electrocorticogram (ECOG) spectral edge frequency (SEF, Hz) spiking pattern.

ECOG SEF, FHR and fetal arterial blood pressure (ABP, mmHg) are shown during a 10 minutes segment demonstrating the correlated changes in FHR decelerations and ECOG SEF spiking pattern during each umbilical cord occlusion (UCO, indicated by the black bars). Note pathological decreases of ABP during the FHR decelerations.