Chapter 11 – Fetal Compromise




Abstract




Key Implications





Chapter 11 Fetal Compromise Diagnosis and Management


Anna Gracia Perez-Bonfils and Edwin Chandraharan




Key Facts




  • Increasing strength, frequency and duration of uterine contractions during labour may reduce oxygenation to the utero-placental bed, increasing the risk of intrapartum hypoxia.oIntrapartum hypoxia and subsequent metabolic acidosis may lead to short-term complications such as admission to neonatal unit, hypoxic ischaemic encephalopathy (HIE) and neonatal death or long-term implications such as learning difficulties or in the worst case scenario, cerebral palsy. There is a wide range of neurological damage, some of which may not be obvious at birth, but may manifest later as functional disabilities.



  • According to current scientific evidence, the vast majority of fetuses are damaged antenatally or postnatally. Intrapartum hypoxia accounts for up to 30% of all cases of cerebral palsy and long-term neurological sequelae.



  • Fetuses with chronic utero-placental insufficiency (intrauterine growth restriction), congenital or acquired infection (chorioamnionitis) or pre- or post-maturity may have less physiological reserves to deal with intrapartum hypoxic insults.



  • Intrapartum sentinel hypoxic events such as uterine scar dehiscence (or rupture), placental abruption or cord prolapse may cause acute hypoxic injury.



  • The main aim of fetal monitoring is to timely identify and hence salvage fetuses that are at risk of intrapartum hypoxic injury, while avoiding unnecessary operative intervention to fetuses who are normoxic or those who are mounting a good compensatory response.



  • As a test of intrapartum hypoxia, cardiotocograph (CTG) interpretation based purely on pattern recognition has a very high false positive rate (approximately >90%). There is a significant intra- and inter-observer variation and the positive predictive value of abnormal features of a CTG for intrapartum hypoxia is less than 30% [1, 2]. Since its introduction into clinical practice in late 1960s there has been an increase in operative interventions during labour without any noticeable reduction in the rates of perinatal deaths or cerebral palsy.



  • Except in cases of acute hypoxia, management decisions should not be taken based on CTG patterns alone. Interventions should be based on understanding the wider clinical picture, fetal reserves and compensatory mechanisms.



  • According to a Cochrane systematic review in 2017 [3], compared with intermittent auscultation, continuous cardiotocography showed no significant improvement in overall perinatal death or cerebral palsy rates but was associated with halving neonatal seizure rates. There was an increase in caesarean sections and instrumental vaginal births. Intermittent auscultation therefore is appropriate for use in the low-risk setting.



Key Implications




  • The cardiotocograph (CTG) has been used for fifty 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 CP has remained fairly stable over the last 50 years, whereas there has been a significant increase in the incidence of operative delivery since the introduction of CTG [3].



  • The 4th Confidential Enquiries into Stillbirths and Deaths in Infancy (CESDI) report in 1997 [4] concluded that issues with interpretation and failure to act when a CTG abnormality was detected may have contributed to more than half of all intrapartum related deaths.



  • Lack of knowledge to interpret CTG traces, failure to incorporate the wider clinical picture (meconium staining of amniotic fluid, intrapartum bleeding, maternal pyrexia, pre- and post-maturity), failures in communication and team working as well as delay in action contribute to intrapartum injury [5] (see Figure 11.1).



  • CTG interpretation based on ‘pattern recognition’ leads to unnecessary interventions as well as lack of action, as all the CTG patterns of fetal neurological injury are not currently known. Moreover, the ‘specific’ CTG patterns are not consistently present in all cases.



  • It is therefore essential to understand the pathophysiology of intrapartum fetal hypoxia to improve outcomes and to reduce unnecessary interventions, rather than reacting to ‘CTG patterns’ [6].



  • The STAN (ST Analyser) is a technology developed to assess the oxygenation of the fetal heart that notifies the switch to anaerobic metabolism in the myocardium secondary to an ongoing hypoxia. A recent meta-analysis including six randomised controlled trials (26,446 women) concluded that there was a 36% reduction in the rate of neonatal metabolic acidosis when using STAN. In addition, there was a statistically significant reduction in operative vaginal delivery rate and the use of fetal blood sampling [7].



  • Two randomised controlled trials have recently been conducted to determine whether the use of a decision support software to assist the interpretation of CTG improves perinatal or maternal outcomes. The INFANT (INtelligent Fetal AssessmeNT) trial included 46,042 women and the results did not support the hypothesis. The FM alert trial (a randomised clinical trial of intrapartum fetal monitoring with computer analysis and alerts versus previously available monitoring) included 7730 women and access to computer analysis of CTGs resulted in the lowest incidence of newborn metabolic acidosis ever reported in randomised controlled trials, but the difference was not statistically significant. Therefore, current scientific evidence does not support the use of computerised CTG interpretation during labour [8, 9].





Figure 11.1 The CTG complexogram.


Source: Ref. [5].


Key Pointers




  • Recognition of the fetus that is at an increased risk of intrapartum hypoxic insult:



  • Prematurity and postmaturity, intrauterine growth restriction, maternal disorders (severe preeclampsia, diabetes mellitus, immunological disorders such as systemic lupus erythematosus), maternal infections including pyrexia with or without clinical chorioamnionitis.



  • Recognition of markers of sentinel hypoxic events during labour: fresh thick meconium, intrapartum bleeding, prolonged or sudden cessation of uterine contractions.



  • Erroneous monitoring maternal heart rate is sadly not an uncommon error. High index of suspicion must be exercised to avoid this pitfall. A sudden improvement of the CTG trace with disappearance of decelerations as well as presence of accelerations, especially during the second stage of labour, should raise an alarm.



Key Diagnostic Signs


Intrapartum hypoxia should be suspected when there are changes in the baseline heart rate (i.e. below 110 beats/minute or above 160 beats/minute) and/or presence of decelerations (on auscultation for 1 minute after a uterine contraction) on intermittent auscultation. Similarly, if any of the following risk factors are present (Table 11.1), continuous electronic fetal monitoring (CEFM) using a CTG should be commenced.




Table 11.1 Indications for continuous electronic fetal heart rate monitoring in labour









Maternal problems




  • Any condition that increases the risk of utero-placental insufficiency, including:



  • Induced labour



  • Diabetes



  • Prolonged rupture of membranes (>24 hours)



  • Antepartum haemorrhage (placental abruption)



  • Previous caesarean section (scar dehiscence)



  • Preeclampsia (placental insufficiency)



  • Post-term pregnancy (>42 weeks)



  • Other maternal medical disease (systemic lupus erythematosus, renal disease)


Fetal problems




  • Any condition that reduces fetal blood flow or compromises fetal response to hypoxic insults:



  • Prematurity



  • Oligohydramnios (possible cord compression/utero-placental insufficiency)



  • Fetal growth restriction



  • Abnormal Doppler artery velocimetry



  • Multiple pregnancy



  • Meconium-stained liquor



  • Intrauterine infection


Intrapartum risk factors




  • Events that occur in labour and rapidly reduces fetal oxygenation:



  • Vaginal bleeding in labour (abruption, vasa praevia)



  • Oxytocin augmentation (hyperstimulation)



  • Epidural analgesia (maternal hypotension)



  • Maternal pyrexia (fetal inflammatory damage)



  • Fresh meconium-stained liquor (meconium aspiration syndrome)



  • Any deceleration or abnormal baseline on intermittent monitoring



CTG Interpretation





Figure 11.2 Suggested algorithm for physiological CTG interpretation.



Commencing CTG Monitoring: Getting the Basics Right



The Machine and the Trace

The patient’s details and maternal pulse should be recorded at the beginning of the trace.


Moreover, the date and time on the CTG trace should be checked to ensure it is correct.


It is very important to set the paper speed at the correct rate. In most countries, including the United Kingdom, the paper speed is set at 1 cm/minute, while in the United States is set at 3 cm/minute. If the paper speed is incorrectly set the appearance of the CTG may change. For example, increase in the speed from 1 cm/minute to 3 cm/minute may create an erroneous impression that the variability is reduced. This may result in an incorrect classification and unnecessary intervention.


It is also important to record vaginal examinations, applications of scalp electrode, administration of oxytocin, and so forth so as to optimise interpretation.


If there is any doubt that the machine is recording the maternal pulse instead of the fetal heart rate (e.g. repeated accelerations with increased amplitude and duration of uterine contractions), it is recommended to check maternal pulse to exclude the misinterpretation of maternal heart rate as fetal heart rate .



Interpreting the CTG Trace


When analysing a CTG trace, the one should start from the beginning of the trace, when the fetus is in general less exposed to stress, checking if the baseline is appropriate for gestational age [10]. From there, scrutinise all the progression looking for an increase of the fetal heart rate (FHR), among other changes. Consider the following five features of a CTG trace prior to classification of CTG.



Baseline Fetal Heart Rate

Baseline FHR is the mean FHR rounded to increases of 5 beats per minute (bpm) during a period of 10 minutes. In a term fetus an FHR is considered normal between 110 and 160 bpm.


An increase in the baseline FHR above 160 bpm is called tachycardia and may be physiological in preterm fetus due to the immaturity of the parasympathetic system [11]. In term fetuses it might be secondary to maternal pyrexia or dehydration or rarely due to medications (e.g. betamimetics). Moreover, it can be seen as a fetus attempts to compensate for the ongoing hypoxic stress, as a result of a surge in catecholamines. Therefore, it is mandatory to consider the trend of the baseline FHR over time (and compare it to the FHR recorded at the beginning of the CTG) as well to the absolute number of baseline FHR.


Baseline bradycardia is defined as FHR below 110 bpm lasting for more than 10 minutes. Similarly, a post-term fetus can physiologically have a lower baseline due to parasympathetic overdrive. Attention should be taken to ensure that the heart rate recorded is not the maternal one.



Baseline Heart Rate Variability (‘The bandwidth’ 5–25 bpm)

The ‘bandwidth’ or the variation of the heart rate above and below the baseline on the CTG trace is called baseline fetal heart variability. This reflects oxygenation of the central nervous system (CNS) centres (the sympathetic and parasympathetic) that are responsible for the control of the FHR. The normal baseline variability of 5–25 beats per minute (bpm) implies that cerebral hypoxia is unlikely.



Reduced baseline variability of 0–5 bpm may represent a quiet sleep phase or may indicate depression of the CNS due to causes such as pharmacological agents (CNS depressants), fetal CNS infections, fetal strokes or hypoxia.


An increase in the baseline variability (more than 25 bpm during more than 30 minutes in the absence of decelerations) is termed saltatory pattern’ and should be viewed with caution. This may reflect a rapidly developing intrapartum hypoxic insult that may cause instability to the fetal autonomic nervous system [12, 13].


The sinusoidal pattern (also called typical sinusoidal pattern) is defined as a regular sine-wave oscillation with an amplitude of 5–15 bpm and a reduced or absent baseline variability and deficiency of accelerations, lasting for longer than 30 minutes. It can be seen in a physiological situation such as fetal thumb sucking or pathologically, in association with severe fetal anaemia.


A pattern similar to the sinusoidal but with a more jagged ‘saw-tooth’ appearance has been called ‘atypical sinusoidal pattern or ‘Poole shark teeth pattern’ and can be secondary to acute feto-maternal haemorrhage in ruptured vasa praevia [14]. If suspected, efforts should be made in delivering in the safest and quickest manner.


Pseudo-sinusoidal pattern is the term used by some authorities to describe undulatory waveforms alternating with episodes of normal baseline variability with the presence of accelerations. It is of unknown significance.


A healthy fetus at term will demonstrate active and quite sleep cycles approximately once every 50 minutes. This important physiological phenomenon called ‘cycling’ should be considered while interpreting the CTG. Absence of cycling might occur during hypoxic and none hypoxic causes such chorioamnionitis [15].

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May 9, 2021 | Posted by in OBSTETRICS | Comments Off on Chapter 11 – Fetal Compromise
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