Fetal Monitoring

Best Practice & Research Clinical Obstetrics and Gynaecology 27 (2013) 509536
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Best Practice & Research Clinical Obstetrics and Gynaecology

journal homepage: www.elsevier.com/locate/bpobgyn
Understanding cardiotocographic patterns associated with intrapartum fetal hypoxia and neurologic injury
Austin Ugwumadu, PhD, FRCOG, Consultant and Senior Lecturer in Obstetrics and Gynaecology *
Department of Obstetrics & Gynaecology, St Georges Hospital and University of London, Blackshaw Road, London SW17 0QT, UK
Keywords: intrapartum hypoxic ischaemic brain injury cardiotocograph fetal heart rate monitoring
Widespread use of fetal heart rate monitoring for intrapartum fetal surveillance preceded our detailed understanding of the behaviour and regulation of the fetal cardiovascular system during labour. The fetal heart rate is sensitive to fetal hypoxaemia and hypoxia, but lacks specicity for fetal acidosis, the end point of unmitigated hypoxaemia and hypoxia. Original interpretations of fetal heart rate patterns equated decelerations to fetal distress and mandated operative intervention. Since then, obstetricians have been trained to focus on the morphological appearances of fetal heart rate decelerations rather than to understand the underlying physiological mechanisms, how the fetus compensates and defends itself, and those patterns that suggest progressive loss of compensation. Consequently, operative interventions are commonly undertaken to rescue fetuses that display benign signs of fetal heart rate adaption to events in labour. Failure to recognise abnormal fetal heart rate patterns remains the leading cause of avoidable brain injury and litigation. In this chapter the general characteristics of the fetal heart rate, the changes in fetal heart rate pattern that may occur during labour, and the patterns that suggest failure of the fetal compensatory mechanisms leading to injury are discussed. 2013 Published by Elsevier Ltd.
* Tel.: 44 20 8725 0506/0501; Fax: 44 20 8725 1975. E-mail addresses: augwumad@sgul.ac.uk, ugwumadu@btinternet.com. 1521-6934/$ see front matter 2013 Published by Elsevier Ltd. http://dx.doi.org/10.1016/j.bpobgyn.2013.04.002
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A. Ugwumadu / Best Practice & Research Clinical Obstetrics and Gynaecology 27 (2013) 509536
Basic principles of intrapartum fetal heart rate interpretation Dening a normal or near-normal cardiotocograph during labour The clinical importance of a normal cardiotocograph (CTG) is that it establishes that the fetal neurological and cardiovascular systems are sufciently intact and able to react and respond to defend the fetus against intrapartum insults. Secondly, it is the hallmark of a healthy fetus and symbolises fetal wellbeing,1 normoxia,2 normal fetal acid base status,3,4 absence of asphyxia3,4 and a low probability of developing intrapartum fetal asphyxia,5 barring some obstetric catastrophe. On the other hand, a non-reactive fetal admission test is associated with adverse fetal outcome5 and long-term neurological decit.68 It is reasonable to presume that a fetus with an abnormal CTG cannot be relied upon to display the predictable changes that characterise maladaptative responses to the asphyxiating process of labour; however, no direct evidence currently supports this. A normal intrapartum CTG (Fig. 1) should satisfy the following criteria: (1) it should have a stable baseline fetal heart rate (FHR) of between 110160 bpm without decelerations; (2) it should have normal baseline FHR variability oscillating between 525 bpm above and below the stable baseline FHR; (3) it should also have periods of reduced FHR variability, which alternate with periods of increased FHR variability with or without accelerations, the fetal cycling activity. In contrast to the antenatal period when the presence of accelerations is required to dene a normal CTG, the absence of spontaneous FHR accelerations during labour is entirely acceptable provided that the other CTG features of fetal wellbeing are present. In practice, it is often possible to elicit FHR acceleration by stimulating the fetus. Fetal cycling activity is the fundamental behavioural characteristic of the neurologically normal and non-hypoxic term or near term fetus. Collectively, these CTG features indicate normal fetal behaviour, neurological integrity, and the absence of signicant hypoxia or acidosis. Although some obstetricians and midwives often worry unduly about normal and transient reduction in baseline FHR variability, a quantitatively normal or even increased FHR variability that does not alternate with a quiet period of reduced variability is not normal and should also elicit concern. Fetal cycling activity may be absent in
Fig. 1. A normal cardiotocograph showing a stable baseline fetal heart rate of about 130 bpm without decelerations, normal baseline variability, accelerations, and fetal cycling activity.
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hypoxia, chorioamnionitis, intrauterine fetal infection, exposure to drugs (including oxytocin, sedatives, narcotics, atropine), complete heart block, fetal brain haemorrhage, or malformation such as anencephaly. Fetal heart rate decelerations Put simply, an FHR deceleration is a reex chemoreceptor-mediated parasympathetic response to a brief spell of oxygen deprivation (hypoxic, ischaemic stimulus, or both). It is widely believed that the purpose of this key adaptation is to reduce myocardial work load and oxygen demand.9 Most of the FHR decelerations (85% or more) observed during labour are variable decelerations, characterised by a sharp fall in FHR from the baseline, reaching the nadir in less than 30 s, and vary in depth, shape, duration and temporal relationship with contractions. Over the years, undue emphasis has been placed on these morphological appearances and the lack of relationship with contractions. In practice, however, these characteristics and emphasis do not add value to clinical interpretation or decision making. What matters is the fetal response to the stimuli that generate the decelerations. Early decelerations, as originally described by Hon and Quilligan26 and subsequently by Caldeyro-Barcia27 as type 1 dips are exceedingly rare, and for practical purposes can be largely discounted. Because the socalled early decelerations or type 1 dips were not associated with fetal acidosis, however, many clinicians extrapolated this to mean that decelerations that are synchronous with contractions are early and are therefore benign, with disastrous consequences. Late decelerations lag behind uterine contractions in timing and are caused by impaired oxygen transfer across the placenta. The relevant clinical question to ask whenever decelerations emerge in a previously normal CTG is whether the fetus is compensating appropriately and adequately to the cause(s) and the effects of the decelerations. The answer to this critical question is at the centre of appropriate interpretation and application of intrapartum FHR monitoring. The healthy fetus with a previously normal CTG will display a predictable set and sequence of FHR changes in response to hypoxic ischaemic insults, depending on whether these are slow in onset, mild to moderate and progressive, or acute and profound. The qualitative patterns of these responses are predictable and should form the template for effective and clinically meaningful FHR interpretation. Fetal heart rate variability The FHR variability may be dened as random uctuations in the baseline FHR, which are irregular in amplitude and frequency. These uctuations are induced by the abrupt but normal changes in the
Fig. 2. The relationship between hypotension and neuronal damage. The severity of fetal systemic hypotension during asphyxia induced by partial uterine artery occlusion is closely related to the degree of neuronal loss and risk of death in the near term fetal sheep.
Fig. 3. (af) The progression from a normal cardiotocograph through a slowly evolving hypoxia process. Fetal heart rate decelerations are the rst cardiotocograph abnormality to appear followed by a rise in the baseline fetal heart rate and then loss of variability. Recovery follows the same sequence. If the cause is not corrected, the baseline fetal heart rate declines to a terminal bradycadia. The disappearance of accelerations if present initially will precede these changes.
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Fig. 3. (continued)
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Fig. 4. (ad) Fetal heart rate progression through a subacute hypoxia process. This pattern is characterised by deep, long-lasting fetal heart rate deceleration associated with brief and progressively diminishing recovery time at baseline. This pattern is associated with rapid decline in pH and the baseline fetal heart rate may be normal.
interval between consecutive heart beats. In clinical practice, FHR variability is assessed visually and quantied as the amplitude of peak-to-trough in beats per minute. The origin of the FHR variability is complex, with inputs from other cycling physiological systems. The fetus requires integrity of the cerebral cortex, midbrain, vagus nerve, and the cardiac conductive tissues to exhibit normal FHR variability. The fetus with a normal FHR variability is at a low risk of immediate death or brain injury caused by asphyxia, regardless of the presence of decelerations or bradycardia.10 On the other hand, a
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Fig. 4. (continued)
reduction or absence of FHR variability was reported to be an important indicator of fetal hypoxia and evolving acidaemia in term11,12 and preterm fetuses.13 A recent systematic review14 suggested that the most consistent predictor of newborn acidaemia was minimal or undetectable FHR variability,14 although animal experiments have also shown increased FHR variation with the onset of severe acidosis and hypotension in one-third of term-equivalent fetal sheep subjected to repeated brief umbilical cord occlusions.15
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Fig. 5. Non-asphyxial prolonged fetal heart rate decelerations with nadir hovering around 60100 bpm and brief loss of variability: (a) normal variability maintained, (b)nadir less than 80 bpm with loss of variability but complete recovery; (c and d) show acute fetal heart rate decelerations from antecedent pathological cardiotograph; (e) the prognosis here is worse compared with fetal heart rate collapse from a completely normal trace.
A number of key clinical conclusions may be drawn from the above discussions: (1) during labour, and in the presence of FHR decelerations, intermittent or sustained reductions in FHR variability may signal the onset of decompensation, unless fetal asphyxia could be excluded; (2) in the presence of normal FHR variability, the role of fetal blood sample is limited16,17; (3) a fetus with a previously normal FHR variability will not switch to one with reduced or absent variability without the input of asphyxial FHR decelerations; (4) if the FHR variability is absent at the outset of monitoring, then it is impossible
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Fig. 5. (continued)
to distinguish between asphyxial and non-asphyxial causes of decreased FHR variability without determination of fetal acid base status. Fetal cardiovascular responses to intrapartum oxygen deprivation As the constant supply of oxygen is essential for the production of cellular energy and maintenance of cellular integrity (in essence for life itself), the cardiovascular system is programmed to rapidly
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Fig. 5. (continued)
detect, assess, and redress any form of oxygen deprivation. The sole aim of this response is the centralisation of the circulation to maintain perfusion of the essential organs the brain, the myocardium, and the adrenals at the expense of the non-essential organs, such as the lungs, skin, muscles, liver, kidneys, and the gastrointestinal tract. The response is initiated by the rapid response neural chemoreexes in the immediate to short term, and subsequently augmented by the slower acting endocrine, endothelial and behavioural responses in the medium to long term.18,19 Once activated, the chemoreex response is qualitatively similar but quantitatively different across insult paradigms, and is nely calibrated to produce varied responses, depending on the severity of the insult and the cellular tolerance of the host. Hypoxic insults that are slow in onset and persistent over time allow the fetus to make homeostatic adaptations, including metabolic adjustments, and elicit different FHR patterns. Experimental studies in fetal sheep have shown that the fetus can sustain its protective cardiovascular system adaptations during prolonged hypoxaemia in the absence of progressive metabolic acidaemia.2022 These protective adaptations begin to fail with the development of acidaemia; at pH less than 7.0, the entire fetal and cerebral oxygen consumption fall substantially. Acidaemia leads to loss of vascular tone, cardiac cell injury, depressed myocardial function, and hypotension with resultant ischaemic brain injury (Fig. 2).24,25 On the other hand, Clapp et al.23 showed that signicant neurological injury can be produced in the sheep model with intermittent cord compression, irrespective of acidosis or encephalopathy.23 Within the brain, regional distribution of ow shunts blood away from the cortex to the deep nuclei and brain-stem structures. In contrast, during total profound asphyxia (e.g. massive abruption, total cord occlusion or uterine rupture) fetal pO2 rapidly reduces within minutes, resulting in an initial rapid chemoreex-mediated generalised vasospasm, followed by hypoxic decompensation and nally profound systemic hypotension and brain infarction in such quick successions that regional redistribution of blood within the brain is unsuccessful in protecting the deep structures. In the dramatic cases the reduced cardiac output and hypotension result in such profound and prolonged FHR deceleration, that circulatory centralisation and regionalisation of blood ow within the brain fail, leading to injuries in the vulnerable regions of the brain before other systemic organs. Intrapartum cardiotogograph patterns associated with fetal hypoxia and neurologic injury During labour, an intact fetus with a previously normal CTG will inevitably exhibit a predictable sequence of FHR responses after the emergence of hypoxic ischaemic insults, depending on the nature
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and severity. The patterns of these FHR responses are reliable predictors of the patterns of potential brain injury that may result if they were allowed to persist. Four distinct patterns of intrapartum hypoxia are commonly encountered during labour, namely slowly evolving hypoxia; subacute hypoxia; acute hypoxia; and chronic (or pre-existing) hypoxia. It is my rm belief that recognition of these patterns is essential to effective management and the prediction of the resultant brain injury. In some instances, there may be dual insults, which may be sequential with characteristic overlapping injury types. Slowly evolving hypoxia With a normal CTG, the onset of intermittent episodes of oxygen deprivation or hypoxaemia results rst of all in the appearance of decelerations associated with uterine contractions (Fig. 3a and b). The amplitude and duration of the decelerations depend on the severity and duration of the hypoxic stress or insult. During labour, this is usually caused by cord compression, and sometimes may follow injudicious use of oxytocin. Persistence or more likely progression of these insults results in a second change in the CTG manifested as an increase in the baseline FHR, usually to about 160180 bpm (Fig. 3c) as the baby increases his cardiac output via an adrenaline surge to deal with the stressful stimuli. Unlike adults, the fetus cannot increase its stroke volume signicantly, and therefore relies almost entirely on raising its FHR to increase its cardiac output. Therefore, a sustained FHR tachycardia in association with uterine contractions is a sensitive marker of a compensatory increase in fetal cardiac output (Fig. 3 c and d). It is widely believed that the fetal cardiac output does not change in the absence of signicant acidaemia. The duration of time that babies can spend at their maximum FHR without damage is variable, and depends on the individual babys reserve. Fleischer et al.28 showed that, in well-grown term fetuses in spontaneous labour with clear liquor and a previously reactive CTG, the average time taken for 50% of them to develop acidosis depended on the type of decelerations present, and was 115 mins with repeated late decelerations, 145 mins with variable deceleration, and 185 mins with at and nonvariable trace.28 Needless to say, that these threshold times do not apply to fetuses with reduced physiological reserve, including intrauterine growth restriction, thick meconium, or infection, and that acidosis may develop earlier. The critical factor here is that slowly evolving hypoxia is gradual in onset and allows the fetus time to make cardiovascular system and metabolic adjustments and that, in the absence of progressive metabolic acidaemia, the fetus can sustain its protective circulatory adaptations almost indenitely.2022 As outlined above, however, these protective adaptations will begin to fail with the development of acidaemia. At birth, the baby, subjected to slowly evolving hypoxia, is likely to exhibit signs of multi-organ dysfunction, including abnormal liver and kidney function consistent with the longstanding withdrawal of blood ow to these organs to protect the essential organs from hypoxia. The third CTG abnormality to be observed if the noxious stimulus was not removed is reduction or lack of baseline variability (Fig. 3d and e). Finally, as the fetal myocardium begins to tire from the persistent lack of oxygen, the FHR falls gently towards a terminal bradycardia (Fig. 3e and f). Wellgrown, normal, term fetuses in spontaneous labour with clear liquor and a previously normal CTG would take at least 1 h to transit through and display these changes. Subacute hypoxia Subacute hyoxia is characterised by complicated variable decelerations, with the amplitude of the deceleration 60 bpm or more and lasting for 90 s or more. When the babys FHR returns to its baseline, it spends less than 60 s before the onset of the next deceleration (Fig. 4 ad). The brief duration of time spent at the baseline FHR during recovery is insufcient to rid the fetus of its CO2 burden accumulated during the preceding deceleration lasting 90 s or more. Therefore, a rapidly cumulative build up of CO2 takes place and initially respiratory but subsequently metabolic acidosis. The actual baseline FHR may be within the normal range of 110160 bpm, as the fetus is unable to raise its baseline FHR because of the brief time at the baseline after recovery before the onset of the next deceleration. Subacute hypoxia is associated with a rapid decline in pH, usually at the rate of
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Fig. 6. (ai) Pre-existing hypoxia and brain damage. Note the reduced variability and absence of fetal cycling activity. The initial lack of decelerations in response to uterine contractions suggest that there was no ongoing intrapartum hypoxia. The baby was markedly depressed at birth.
0.01 every 24 mins, in contrast to the slowly evolving hypoxia process where the rate of fall of the pH is usually much more slowly. Compared with slowly evolving hypoxia, the relatively rapid progression to, and development of, metabolic acidaemia during subacute hypoxia means that the transition to acidaemia sufcient to exert the loss of vascular tone, depressed myocardial function and hypotension with resultant ischaemic
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Fig. 6. (continued)
brain injury may also be rapid. In clinical practice, the recognition of this pattern is crucial as, once subacute hypoxia is established, there is likely to be insufcient time to obtain, analyse and react to a fetal blood sample result without the risk of incurring damaging severe acidaemia. Acute hypoxia (prolonged fetal heart rate deceleration and bradycardia) As baseline FHR 100 -109bpm (suspicious) and <100bpm (abnormal) even with the recent revisions and temporal qualications such as single prolonged deceleration (3 minutes or more but less than 10 minutes), and bradycardia >10 minutes. The denition of FHR bradycardia by the UK National Institute for Clinical Excellence is baseline FHR 100109 bpm (suspicious) and less than 100 bpm (abnormal). Even with recent revisions and
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Fig. 6. (continued)
temporal qualications (e.g. single prolonged [3 mins or more] and single prolonged deceleration [10 mins or more]), this guidance is still open to misinterpretation during labour. Most acute-onset intrapartum FHR decelerations, in which the baseline FHR stabilises around 80100 bpm with the variability maintained, are due to non-asphyxial vagal events.29,30 Most of these arise out of a previously normal or near normal CTG traces. In the absence of an obstetric catastrophe, such as cord prolapse or occlusion, major abruption, uterine rupture, infusion of a bolus of oxytocin, or maternal collapse, 90% of these episodes will recover, or at least show signs of recovery, by 6 mins, whereas 95% of them should have recovered or be recovering by 9 mins (Fig. 5a and b).31 It is therefore reasonable to manage these expectantly or transfer them back from theatre if the journey was already made hastily. The mother should be tilted to the left side and rehydrated if hypotensive. The
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Fig. 6. (continued)
situation is somewhat different if the FHR dropped to less than 80 bpm for more than 3 mins with loss baseline variability (Fig. 5c and d). In my opinion, delivery should be considered. The sudden onset and persistent loss of variability may be a possible sign of fetal decompensation and possibly fetal injury. Although some of the cases with this pattern do recover (Fig. 5e), many do not. These decelerations are probably associated with unidentied pathological processes. Other related situations include a profound FHR bradycardia as part of a declining FHR after a prolonged period of slowly evolving hypoxia process or FHR collapse after a period of subacute hypoxia. In both scenarios, the risk of neurological injury is high within a relatively short period of time related to the preexisting compromised status of the fetus, probably caused by established fetal acidaemia, hypotension, or both. During acute profound asphyxia, fetal pO2 falls rapidly, resulting in a rapid chemoreexmediated generalised vasospasm aimed at centralising blood ow to maintain central organ
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Fig. 6. (continued)
perfusion. The lack of oxygen and substrates quickly leads to energy failure, hypoxic decompensation, and profound systemic hypotension and brain infarction. For the same reasons, regional redistribution of blood within the brain is also unsuccessful in protecting the deep structures. The highly metabolic deep nuclei are therefore damaged as well as cortical and watershed areas of the brain. Pre-existing hypoxia or neurological injury The utility of intrapartum FHR monitoring to improve perinatal outcomes is based on the premise that fetuses have not been exposed to prolonged antenatal hypoxia and resultant neurological injury before the onset of labour. This is true for most fetuses; however, severe antenatal hypoxia is not uncommon32,33 and may present with FHR abnormalities in human fetuses34 and in animal models.35,36 Although fetuses with antecedent hypoxic ischaemic brain injury do not display a set of uniform FHR abnormalities, they do show distinct FHR patterns on admission and subsequent intrapartum changes that permit an accurate diagnosis of their status. The typical FHR pattern in fetuses with pre-exiting hypoxia or neurological injury is characterised by a xed and relatively invariable baseline rate, with reduced to average, but constant, variability that does not exhibit fetal cycling activity (Fig. 6 a f). Sometimes, FHR tachycardia may occur, which is usually more marked above 160 bpm, the more recent the central nervous system insult or normal FHR 110160 bpm to marginal tachycardia the more remote from admission the central nervous system insult.34 Unlike the three FHR patterns associated with evolving and ongoing intrapartum fetal hypoxia described above, this pattern represents a static encephalopathy, which cannot be modied signicantly by aggressive operative intervention. If the fetus still has a residual hypoxia after the insult, or has developed an ongoing intrapartum hypoxaemia, there will be FHR decelerations in response to uterine contractions. These are typically shallow and low in amplitude. In the absence of acidaemia, the CTG will show absence of decelerations despite the brain damage. At birth, these babies have raised nucleated red blood cells,37,38 prolonged nucleated red blood cells clearance times,37,39 suggestive of antecedent hypoxic insult, multi-organ system
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Fig. 7. (ai) This pregnancy was induced for postdate and initially showed lack of fetal cycling activity and reduced variability for many hours, with a meconium stained liquor. The mother had epidural analgesia and ran temperatures 390C and higher, leading to fetal heart rate tachycardia. The absence of fetal heart rate decelerations suggest that the problem was non-hypoxic in origin until panel 7j onwards. The baby was born severely depressed by a difcult caesarean section after a failed forceps attempt and died after 10 h. Postmortem revealed intrauterine pneumonia (Staphylococcus aureus) and hypoxic ischaemic brain injury, most likely exerted by synergistic inammatory and hypoxia ischaemia. Membranes stripping was undertaken a few days earlier, and it is conceivable that the membranes might have been inoculated in the process with S. aureus.
dysfunction,39 delayed onset of seizures,40 cortical brain injuries,7 old meconium, meconium aspiration syndrome, and pulmonary hypertension.6 Severely growth restricted babies are disproportionately represented in this group. Compared with their appropriately grown peers, they develop acidaemia more easily and display more brief bradycardia, a quicker FHR return to baseline after exposure acute hypoxaemia,41 and tachycardia with recovery, attributed to increased sympathetic tone.42
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Fig. 7. (continued)
Infection, inammation, and fetal heart rate abnormalities Chorioamnionitis may progress to a generalised fetal inammation, called the fetal systemic inammatory response syndrome,43 which is mediated in part by widespread endothelial injury.44 The fetal systemic inammatory response syndrome is associated with hypotension, neonatal seizures, need for intubation, meconium aspiration syndrome, multi-organ dysfunction, low Apgar scores, neonatal depression, hypoxic ischaemic (and non-hypoxic) neonatal encephalopathy,4547 intraventricular haemorrhage,48 white-matter damage, periventricular leucomalacia, bronchopulmonary dysplasia, and cerebral palsy.49 Yet, no reliable tools are available to identify fetuses at
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Fig. 7. (continued)
increased risk of infection-driven encephalopathy or brain injury. Current intrapartum electronic FHR monitoring technology lacks sufcient sensitivity to detect fetal systemic inammatory response syndrome, placental inammation, or predict neonatal sepsis.50 We know little about what FHR changes are induced by infection either alone or in conjunction with hypoxia. Tachycardia, reduced variability, lack of cycling, or both, may occur (Fig. 7aJ), but none of these is a consistent nding. For example, in fetuses less than 32 weeks gestation, severe variable decelerations and reduced variability were associated with histological evidence of acute inammation, but this nding was inconsistent.51 Sameshima et al.52 showed that, in fetuses with bacterial infection, fetal tachycardia (but not deceleration types) was associated with increased risk of
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Fig. 7. (continued)
cerebral palsy without acidaemia or CTG evidence of bradycardia,52 suggesting that infection may be exerting neurological injury directly or via an alternative non-hypoxia pathway. Variable FHR responses were also observed in experimental animals exposed to infection, and when hypoxia did occur it was usually not associated with acidosis. A further complicating factor is the synergistic interaction between fetal inammation and hypoxia. Strong epidemiological evidence shows that the risk of encephalopathy and cerebral palsy increased exponentially with combined exposure of the fetus to infection and birth asphyxia. It seems that inammation53 may sensitise the immature fetal brain to damage by lowering the threshold at which hypoxia triggers neuronal apoptosis.5457 Fetuses primed in this way may not tolerate even modest degrees of hypoxia inherent in normal labour.
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Fig. 7. (continued)
How then should obstetricians monitor and manage these cases given that the CTG traces in most cases of fetal infection may appear normal or near normal? Firstly, to ensure a good outcome, it is essential to maintain a high index of suspicion and recognise that there are no reliable or predictive tools or combination of tools designed to detect injury in the infected fetus. Secondly, although there is no evidence for routine caesarean section for suspected or proven intrauterine infection as the timing of fetal injury is unknown, the threshold for operative delivery should be lowered if there are co-existing antenatal or intrapartum risk factors such as meconium stained amniotic uid, fever, FHR abnormalities, intrauterine growth restriction, or antepartum
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Fig. 7. (continued)
haemorrhage. For example, in one study, the relative risk of fetal infection was 50-fold greater if fetal tachycardia was associated with meconium stained liquor,57 especially in early labour. Intrapartum pyrexia, even of non-infectious origin, is associated with increased risk of neonatal seizures.58,59 Therefore, fetal infection is present, clinicians should avoid intrapartum factors that may amplify the risk of synergistic brain injury such as prolonged labour, injudicious use of oxytocics and uterine hyper-stimulation, and traumatic operative vaginal deliveries.60 It is misguided to use tests such as the CTG, fetal blood sample, fetal electrocardiography waveform analysis, pulse oximeter, which are designed for detection of fetal hypoxia to clarify fetal wellbeing in the presence of infection or inammation.60
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Fig. 7. (continued)
Inadvertent monitoring of the maternal heart rate The maternal heart rate has similar, if not identical, characteristics as the FHR, and could easily be mistaken for it, especially if maternal tachycardia is present. During the active phase of the second stage of labour, the FHR may collapse and the CTG machine may pick up and display pulsations from a maternal abdominal or pelvic vessel. This can also occur if there are maternal movements or cord compression. The observer should be able to recognise the characteristic MHR tracing during the active second stage of labour, typically consisting of gigantic broad accelerations coinciding with the peaks of uterine contractions and maternal bearing down efforts (Fig. 8). The clue is in the near perfect alliance between the onset and offset of the accelerations with the onset and offset of the uterine contractions respectively.61 A closer and systematic assessment of the CTG
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Fig. 8. Characteristic maternal heart rate tracing during the active second stage of labour showing broad accelerations coinciding with the peaks of uterine contractions and maternal bearing down efforts. A near perfect alliance can be seen between the onset and offset of the accelerations with the onset and offset of the uterine contractions, respectively.
will reveal accelerations with the contractions, which is neither physiological nor normal fetal behaviour in active second stage of labour. The severe neonatal depression is usually inconsistent with the CTG recording.
Uterine hyperstimulation (oxytocin and prostaglandins use) The medicolegal issues around the use of oxytocin infusion and FHR monitoring may be summarised as follows: (1) starting oxytocin with thick meconium and scanty amniotic uid, chorioamnionitis, suspicious or pathological CTG; (2) failure to recognise or act to reduce uterine contractions greater than 5 in 10 mins by reducing or stopping oxytocin or failure to use tocolytics to alleviate tonic or frequent uterine contractions early; (3) the fetus may be affected with hypoxia despite prompt action. The doctor or midwife, however, may still be liable if the prolonged FHR abnormality was caused by uterine hyperstimulation; (4) cessation of FHR monitoring or uterine contractions much earlier than the time of delivery, such that the baby may be asphyxiated in the interim. Oxytocin increases the amplitude, frequency, and duration of existing uterine contractions, thereby impeding the ow of oxygenated blood into the intervillous space with resultant FHR abnormalities (Fig. 9). Therefore, continuous FHR monitoring is mandatory when oxytocin infusion is in use and during induction of labour with prostaglandins. Oxytocin-induced hyperstimulation features commonly in obstetric negligence claims. Some doctors and midwives seem to be unaware that the uterus is more sensitive to oxytocin as labour progresses and that, during the late rst, and second stages of labour, additional uterine activity occurs owing to Ferguson reex (a positive feedback reex in which pressure on the cervix, the vagina, or both, by the presenting part of the fetus results in uterine contraction). Therefore, dosage increments and contraction frequency must be monitored meticulously, especially with induced labour, as there may still be some residual effects of prostaglandins.
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Fig. 9. Hyperstimulation syndromes. Uterine tachysystole with fetal heart rate decelerations and loss of variability: (a) contraction frequency 8 or more in 10 mins, and (b) a similar example induced by prostaglandin, which was removed about 8 mins from the end of the recording.
Conclusion Appropriate interpretation of intrapartum FHR output requires an in-depth understanding of normal fetal neurological behaviour, the behaviour of the fetal CVS in response to different degrees of hypoxicischaemic insults, the changes that indicate decompensation, and an acceptance that nonhypoxic fetal injuries are common and not necessarily detectable by current FHR monitoring tools or practice. Negligent practices during intrapartum fetal monitoring may result in brain damage and cerebral palsy, and generate high-value claims. Recurring themes feature in most cases of CTG misinterpretation.
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Practice points Intrapartum fetal surveillance should be approached from a physiological stand point rather than a focus on morphological appearances of FHR decelerations. In the absence of antecedent FHR decelerations, isolated FHR tachycardia or reduction in variability are unlikely to be caused by intrapartum hypoxia. In the absence of an obstetric catastrophe, most acute FHR decelerations from a normal CTG and good variability are non-asphyxial and should recover. No reliable or predictive tools, or a combination of tools, have been designed to detect injury in the infected fetus, and sophisticated clinical judgement is required. The fetus with a normal FHR variability is at a low risk of asphyxia or injury regardless of the amplitude and morphology of the FHR decelerations.
Research agenda Digitisation of the FHR and role of computerised systems. Fetal neurological injuries without acidaemia. Timing of injury in infection. What FHR patterns correlate with fetal inammation.
References
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Best Practice & Research Clinical Obstetrics and Gynaecology 27 (2013) 509536

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Best Practice & Research Clinical Obstetrics and Gynaecology

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