Introduction
Intrapartum hypoxia and subsequent metabolic acidosis is associated with short term complications such as admission to neonatal unit, hypoxic ischaemic encephalopathy (HIE) and neonatal death or long term implications such as cerebral palsy or learning difficulties. The main aim of fetal monitoring is to timely identify and hence to salvage fetuses that are at risk of intrapartum hypoxic injury, whilst avoiding unnecessary operative intervention to fetuses that are normoxic.
Cardiotocograph (CTG) has been used for over 40 years to identify intrapartum hypoxia and when CTG was introduced into obstetric practice it was hoped that it would help reduce the cerebral palsy (CP) rate. Unfortunately, the incidence of cerebral palsy has remained fairly stable over the last 40 years whereas, there has been a significant increase in the incidence of operative delivery, since the introduction of CTG. The 4th Confidential Enquiries into Stillbirths and Deaths in Infancy (CESDI) Report concluded that issues with interpretation and failure to act when a CTG abnormality was detected may have contributed to over half of all intrapartum related deaths1. It is therefore essential to understand the pathophysiology of intrapartum fetal hypoxia to improve outcomes2 and to explore better techniques of fetal assessment during labour.
Problems with traditional tests used for intrapartum fetal monitoring
Cardiotocograph (CTG) has been used all over the world over the last 40 years to timely identify fetuses experiencing intrapartum hypoxic insults so that appropriate intervention could be taken to avoid cerebral injury. However, this test has several flaws.
a. Pattern Recognition
CTG relies on pattern recognition and information management by midwives and obstetricians. Unfortunately, not all patterns that are associated with intrapartum fetal hypoxia are currently known. There is a vast degree of inter-observer and intra-observer variation in pattern recognition. The 4th CESDI Report concluded that lack of knowledge to interpret CTG traces was a major contributor to potentially avoidable intrapartum related deaths.
b. High false positive rate and poor positive predictive value of CTG for intrapartum hypoxia
CTG has a very good sensitivity but a very poor specificity and positive predictive value for intrapartum hypoxic injury. Hence, the false positive rate is high. This means that even if CTG shows all the ‘abnormal features’ such as late decelerations, complicated baseline tachycardia and complicated variable decelerations, only 40-60% of fetuses actually have intrapartum hypoxia3. In other words, if operative intervention is undertaken, based on the observed CTG changes alone, 40-60% of fetuses will be born with normal cord blood gases without any evidence of metabolic acidosis. Positive predictive value of a pathological CTG for metabolic acidosis is approximately 30%4. This implies that if a clinician uses the CTG alone for intrapartum fetal monitoring, it is likely that unnecessary operative interventions will be increased without any discernable benefit to perinatal outcome.
c. Requirement for additional tests of fetal wellbeing
In view of its very poor positive predictive value for metabolic acidosis and a high false positive rate, CTG requires additional tests of fetal wellbeing such as fetal scalp blood sampling, (FBS), fetal scalp lactate, fetal pulse oximetry and fetal electrocardiograph (fetal ECG also called STAN or ST-analyser).
d. Problems with CTG Classification
Six years after publication of the 4th CESDI Report that highlighted substandard care (which included lack of knowledge and failure to interpret CTG traces) in over 50% of babies who died due to intrapartum related causes, the Royal College of Obstetricians and Gynaecologists (RCOG) and National Institute of Health and Clinical Excellence (NICE) produced National Guidelines on Electronic Fetal Heart Rate monitoring (EFM) in 20015. This was a very welcome and much needed step in the right direction and it created a platform for universal classification of CTG into Normal, Suspicious and Pathological categories. Hence, varied terminologies such as ‘good CTG’ ‘optimal CTG’, ‘sub-optimal CTG’, ‘bad CTG’, ‘non-reassuring CTG’ etc, which caused much confusion among clinicians in the past, were avoided. However, this classification itself was riddled with many drawbacks. First of all, it over-simplifies the complex process of labour and assumes that there could be only three types of decelerations during labour (early due to head compression, variable due to cord compression and late due to utero-placental insufficiency). There has been no consideration to multiple events such as head and cord compression occurring together during uterine contractions or the importance of fetal reserve or its capacity to respond to hypoxia on the ultimate outcome.
Moreover, clinicians often reacted to ‘CTG Patterns’ described in the EFM Guidelines without considering the clinical picture. Electronic Fetal Monitoring Guidelines was subsequently revised by NICE in 2007 to include a ‘time frame’ for decelerations in order to reduce the likelihood of clinicians reacting and thereby instituting an unnecessary interventions to specific patterns noted in the CTG6. Hence, instead of intervening when one or two late decelerations are noted, the current classification allows late decelerations for 50% of contractions for up to 30 minutes to be present prior to be considered as an abnormal feature. Although, this is a vital step in the right direction, there has been no consideration of the type of hypoxia during labour (acute, sub acute, gradually evolving) or emphasis of other features such as pseudo-sinusoidal patterns, saltatory patterns, loss of cycling of fetal heart rate that may also reflect fetal compromise, in the current NICE Classification.
| Figure 1. Fetal ECG Complex |
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Role of fetal ECG in intrapartum fetal monitoring
Fetal electrocardiograph (ECG) refers to a graphic record of the summation of electrical activity of the myocardial cells. This in turn reflects oxygenation status of a central organ (i.e. myocardium of the heart), which is protected until very late stages of hypoxia by a fetus that mounts a compensatory response to lack of oxygen. Hence, indirectly, it provides informa