Fetal Decompensation Research Articles

Longitudinal changes in the ductus venosus, cerebral transverse sinus and cardiotocogram in fetal growth restriction.

To evaluate the changes in flow velocity waveforms in the transverse cerebral sinus in growth-restricted fetuses and to correlate these changes with (1) flow velocity waveforms in the ductus venosus and (2) changes in computerized analysis of the fetal cardiotocogram. Fetuses between 22 and 37 weeks' gestation with an estimated fetal weight below the fifth centile were included in this prospective longitudinal study. Doppler measurements of the umbilical artery, descending aorta, middle cerebral artery, transverse cerebral sinus and ductus venosus were recorded. Fetal heart rate was analyzed by a computer system according to the Dawes-Redman criteria. We measured a significant correlation between pulsatility index in the cerebral transverse sinus and in the ductus venosus over the study period and at delivery. There was a negative correlation between these indices and short- and long-term variability of the fetal heart rate. There was a parallel increase in pulsatility in the ductus venosus and the transverse cerebral sinus. These changes were inversely correlated with fetal heart rate variability and preceded fetal distress. Cerebral venous blood flow in IUGR fetuses may be a useful additional investigation to discriminate between fetal adaptation and fetal decompensation in chronic hypoxemia.

INTRAPARTUM FETAL SURVEILLANCE: Is It Worthwhile?

Potentially significant intrapartum fetal asphyxia occurs in approximately 20 per 1000 births. Moderate and severe fetal asphyxia exposure with newborn morbidity occurs in 3 to 4 1000 births, with brain damage and subsequent disability in at least 1 per 1000 births. Although the prevalence of moderate and severe asphyxia is modest, prevention is important because of the serious implications of this complication to the child, family, and society. Because of the limited predictive value of clinical risk factors, the interpretation of patterns in a fetal heart rate record has become the primary screening test for intrapartum fetal asphyxia. Despite extensive clinic experience and numerous clinical trials, the benefits of EFM as a screening test have not been established, and harm may occur owing to unnecessary intervention. This observation raises serious ethical issues. When an intervention is initiated by the clinician rather than the patient, the clinician under greater obligation to ensure that the benefits outweigh the harm. Several factors complicate the demonstration of benefits of EFM as a screening test. There is no consensus regarding a protocol of fetal surveillance for low-risk patient who account for approximately 25% of intrapartum fetal asphyxia. Moderate and severe asphyxia cannot be prevented when asphyxial exposure has occurred before labor or before the onset of fetal surveillance. Prediction of intrapartum fetal asphyxia cannot occur when the quality of the record does not permit interpretation. Interpretation of predictive fetal heart rate patterns cannot occur unless the record is consistently and carefully scored. Prediction of most cases of intrapartum fetal asphyxia on the basis of fetal heart rate patterns is possible but difficult. Because the goal of intrapartum fetal surveillance is the prevention of moderate and severe fetal asphyxia, prediction must be achieved before fetal decompensation. Prediction must occur before absent baseline fetal heart rate variability evident in the record, which is uniformly associated with cerebral dysfunction and, in some cases, brain damage. The possibility of fetal asphyxia must be considered when, within a 1-hour window of recording, there are two or more cycles of minimal baseline fetal heart rate variability and two or more cycles of late or prolonged decelerations or both. Because approximately 9 of 10 predictive fetal heart rate patterns are false-positive, supplementary tests to confirm the diagnosis and to identify false-positives to prevent unnecessary intervention are essential. Until such time as additional fetal assessment tests are validated, blood gas and acid-base assessment of fetal blood can provide a definitive diagnosis and identify false-positive predictions.

Fetal heart rate variability changes during brief repeated umbilical cord occlusion in near term fetal sheep.

To determine whether changes in fetal heart rate variation during repeated umbilical cord occlusions reflect evolving cardiovascular compromise in near term fetal sheep. Fetal heart rate variation, fetal mean arterial pressure, electroencephalogram (EEG) and acid-base status were measured during one minute umbilical cord occlusions, repeated either every five minutes (1:5 group) or every 2.5 minutes (1:2.5 group) for four hours or until mean arterial pressure fell below 20 mmHg for two successive occlusions. Fourteen chronically instrumented fetal sheep, mean gestation 126.3 (2.6) days. Cord occlusion caused variable decelerations with initial sustained hypertension. In the 1:5 occlusion group mean arterial pressure remained elevated throughout, with little change in acid-base status (pH = 7.34 (0.07), base deficit = 1.3 (3.9) after 4 hours) and no significant change in fetal heart rate variation. In contrast, in the 1:2.5 group from the third occlusion there was progressive hypotension during occlusions, severe progressive metabolic acidaemia (pH 6.92 (0.1), base deficit 17.0 mmol/L (4.7) after the last occlusion) and marked EEG suppression (P < 0.01). Fetal heart rate variation increased with the onset of occlusions (P < 0.05) and then progressively fell with continued occlusions. During the last 30 minutes of occlusions, fetal heart rate variation was severely suppressed in four, but increased in two fetuses, while all six fetuses developed overshoot-instability of fetal heart rate and mean arterial pressure following each occlusion. Acute progressive asphyxia was typically associated with an immediate, transient increase in fetal heart rate variation. Subsequently variation became suppressed in only two-thirds of fetuses during terminal acidaemia and hypotension. Fetal heart rate overshoot-instability may be a useful marker of fetal decompensation following variable decelerations.

Relationship Between the Fetal Heart Rate Pattern and Perinatal Mortality in Fetuses With Absent End-Diastolic Velocities of the Umbilical Artery

Fetal decompensation is usually diagnosed by the onset of late decelerations and decreased fetal heart rate (FHR) variability and is associated with fetal hypoxemia and acidemia and has a high perinatal mortality. Objective analysis of the FHR pattern can be performed using the Fischer score and a score of less than 6 correlates with fetal decompensation. Fetuses with absent end-diastolic velocities (AEDV) of the umbilical artery have severe placental disease and coupled with this a high perinatal mortality and morbidity. Importantly, AEDV is usually observed before the occurrence of fetal decompensation. In fetuses with AEDV, delivery before decompensation may improve the perinatal mortality and morbidity. To test this hypothesis, the perinatal outcome of fetuses with AEDV delivered before decompensation (Fischer score of 6 or more), were compared with similar fetuses delivered after decompensation (Fischer score of less than 6). All FHR pattern records of fetuses who had AEDV with a birthweight greater than 750 g and a gestational age of 28 weeks or more were evaluated using Fischer's score by a single observer unaware of the perinatal outcome. Fifty-seven fetuses qualified for the study and 17 of these babies subsequently died. The babies who died had significantly lower mean Fischer scores during the preceding 6 hours before delivery (5.9 ± 1.8 SD) than the survivors (7.7 1.9; p <0.05), but also had lower birthweights and gestational ages. To obviate this effect, babies with a Fischer score of less than 6 at 6 hours before delivery (group 1) were matched to within 3 days gestational age and 10% birthweight with those with a Fischer score of 6 or more at 6 hours before delivery (group 2). Nineteen pairs were obtained. There were no differences in perinatal mortality and morbidity between the groups, although the surviving babies in group 1 spent significantly less time in the hospital (p <0.02). Therefore, waiting until a decompensation, as is evident from a low Fisher score, develops does not adversely affect the prognosis of the fetus.

Relationship between the fetal heart rate pattern and perinatal mortality in fetuses with absent end-diastolic velocities of the umbilical artery: a case-controlled study.

Fetal decompensation is usually diagnosed by the onset of late decelerations and decreased fetal heart rate (FHR) variability and is associated with fetal hypoxemia and acidemia and has a high perinatal mortality. Objective analysis of the FHR pattern can be performed using the Fischer score and a score of less than 6 correlates with fetal decompensation. Fetuses with absent end-diastolic velocities (AEDV) of the umbilical artery have severe placental disease and coupled with this a high perinatal mortality and morbidity. Importantly, AEDV is usually observed before the occurrence of fetal decompensation. In fetuses with AEDV, delivery before decompensation may improve the perinatal mortality and morbidity. To test this hypothesis, the perinatal outcome of fetuses with AEDV delivered before decompensation (Fischer score of 6 or more), were compared with similar fetuses delivered after decompensation (Fischer score of less than 6). All FHR pattern records of fetuses who had AEDV with a birthweight greater than 750 g and a gestational age of 28 weeks or more were evaluated using Fischer's score by a single observer unaware of the perinatal outcome. Fifty-seven fetuses qualified for the study and 17 of these babies subsequently died. The babies who died had significantly lower mean Fischer scores during the preceding 6 hours before delivery (5.9 +/- 1.8 SD) than the survivors (7.7 1.9; p < 0.05), but also had lower birthweights and gestational ages.(ABSTRACT TRUNCATED AT 250 WORDS)

The Relationship of Asphyxia in the Mature Fetus to Long-Term Neurologic Function

Asphyxia may occur before or during labor in the preterm or term fetus. The development of neuropathologic lesions depends on the degree and duration of the asphyxia. Anoxia may occur, but because of the short duration of the fetal response, it usually will cause the death of the fetus. The common mechanism leading to neuropathologic lesions in the fetus is a significant degree of hypoxia present for a particular period of time. Antepartum asphyxia will cause such lesions and deficits in children. What is missing are measures to establish the prevalence of antepartum asphyxia in a large population and the epidemiologic studies to determine the association between the asphyxia so documented and the deficits in surviving children. The prevalence of intrapartum fetal asphyxia is of the order of 2%. Most of these children will have no evidence of brain damage. The key is the fetal cardiovascular compensatory response that maintains cerebral blood flow and oxygen metabolism. This compensatory phase, subject to the severity of the hypoxia, may continue for several hours. In the clinical setting during labor, this provides the "window of opportunity" when a specific blood gas and acid-base diagnosis can be made, and with appropriate intervention, brain damage can be avoided. However, if the hypoxia persists, a threshold will be reached when fetal cardiovascular decompensation will occur. The compromised cerebral oxygen metabolism will result in brain damage and deficits in the children who survive. The threshold at which brain damage may occur is when the acidosis is severe (pH, < 7.0). At this time, systemic hypotension may occur.(ABSTRACT TRUNCATED AT 250 WORDS)