Benefits and Limitations of Continuous CTG Monitoring in Labor: Best Practices, Study notes of Literature

Download Benefits and Limitations of Continuous CTG Monitoring in Labor: Best Practices and more Study notes Literature in PDF only on Docsity! FIGO CONSENSUS GUIDELINES ON INTRAPARTUM FETAL MONITORING Safe Motherhood and Newborn Health Committee Co-ordinator: Diogo Ayres-de-Campos CARDIOTOCOGRAPHY Diogo Ayres-de-Campos, Catherine Y. Spong, Edwin Chandraharan, for the FIGO intrapartum fetal monitoring consensus panel. Consensus panel: Daniel Surbek (Switzerland*), Gabriela Caracostea (Romania*), Yves Jacquemyn (Belgium*), Susana Santo (Portugal*), Lennart Nordström (Sweden*), Tulia Todros (Italy*), Branka Yli (Norway*), George Farmakidis (Greece*), Sandor Valent (Hungary*), Bruno Carbonne (France*), Kati Ojala (Finland*), José Luis Bartha (Spain*), Joscha Reinhard (Germany*), Anneke Kwee (Netherlands*), Romano Byaruhanga (Uganda*), Ehigha Enabudoso (Nigeria*), John Anthony (South Africa*), Fadi Mirza (Lebanon*), Tak Yeung Leung (Hong Kong*), Ramon Reyles (Philippines*), Park In Yang (South Korea*), Henry Murray (Australia and New Zealand*), Yuen Tannirandorn (Thailand*), Krishna Kumar (Malaysia*), Taghreed Alhaidary (Iraq*), Tomoaki Ikeda (Japan*), Ferdusi Begum (Bangladesh*), Jorge Carvajal (Chile*), José Teppa (Venezuela*), Renato Sá (Brasil*), Lawrence Devoe (USA**), Gerard Visser (Netherlands**), Richard Paul (USA**), Barry Schifrin (USA**), Julian Parer (USA**), Philip Steer (UK**), Vincenzo Berghella (USA**), Isis Amer-Wahlin (Sweden**), Susanna Timonen (Finland**), Austin Ugwumadu (UK**), João Bernardes (Portugal**), Justo Alonso (Uruguay**), Sabaratnam Arulkumaran (UK**). * nominated by FIGO associated national society; ** invited by FIGO based on literature search The views expressed in this document reflect the opinion of the individuals and not necessarily of the institutions that they represent. 1. INTRODUCTION The purpose of this chapter is to assist in the use and interpretation of intrapartum cardiotocography (CTG), as well as in the clinical management of specific CTG patterns. In the preparation of these guidelines, it has been assumed that all necessary resources, both human and material, required for intrapartum monitoring and clinical management are readily available. Unexpected complications may occur during labour, even in patients without prior evidence of risk, so maternity hospitals need to ensure the presence of trained staff, as well as appropriate facilities and equipment for an expedite delivery (in particular emergency cesarean section). CTG monitoring should never be regarded as a substitute for good clinical observation and judgement, or as an excuse for leaving the mother unattended during labour. 2. INDICATIONS The evidence for the benefits of continuous CTG monitoring, as compared to intermittent auscultation, in both low and high-risk labours is scientifically inconclusive 1-2. When compared to intermittent auscultation, continuous CTG has been shown to decrease the occurrence of neonatal seizures, but no effect has been demonstrated on the incidence of overall perinatal mortality or cerebral palsy. However, these studies were carried out in the 1970s, 1980s, and early 1990s where equipment, clinical experience and interpretation criteria were very different from current practice, and they were clearly underpowered to evaluate differences in major outcomes 3. These issues are discussed in more detail below (see section 8 of this chapter). In spite of these limitations, most experts believe that continuous CTG monitoring should be considered in all situations where there is a high risk of fetal hypoxia/acidosis, whether due to maternal health conditions (such as vaginal haemorrhage and maternal pyrexia), abnormal fetal growth during pregnancy, epidural analgesia, meconium stained liquor, or the possibility of excessive uterine activity, as occurs with induced or augmented labour. Continuous CTG is also recommended when abnormalities are detected during intermittent fetal auscultation. The use of continuous intrapartum CTG in low-risk women is more controversial, although it has become standard of care in many countries. An alternative approach is to provide intermittent CTG monitoring alternating with fetal heart rate (FHR) auscultation. There 2 is some evidence to support that this is associated with similar neonatal outcomes in low-risk pregnancies 4. Intermittent monitoring should be carried out long enough to allow adequate evaluation of the basic CTG features (see below). The routine use of admission CTG for low-risk women on entrance to the labour ward has been associated with an increase in caesarean section rates and no improvement in perinatal outcomes 5, but studies were also underpowered to show such differences. In spite of the lack of evidence regarding benefit, this procedure has also become standard of care in many countries. 3. TRACING ACQUISITION Maternal position for CTG acquisition Maternal supine recumbent position can result in aorto-caval compression by the pregnant uterus, affecting placental perfusion and fetal oxygenation. Prolonged monitoring in this position should therefore be avoided. The lateral recumbent, half-sitting, and upright positions are preferable alternatives 6. CTG acquisition can be performed by portable sensors that transmit signals wirelessly to a remote fetal monitor (telemetry). This solution has the advantage of allowing the mother to move freely during signal acquisition, rather than be restrained to bed or a sofa, and should therefore be the preferred option when available. Telemetry systems differ in the maximum distance allowed between patient and monitor for adequate signal transmission 7. Paper scales for CTG registration and viewing The horizontal scale for CTG registration and viewing is commonly called “paper speed” and available options are usually 1, 2 or 3 cm/min. In many countries throughout the world 1 cm/min is selected, while in the Netherlands it is usually 2 cm/min, and in North America and Japan it is almost exclusively 3 cm/min. Some experts feel that 1 cm/min provides records of sufficient detail for clinical analysis, and this has the advantage of reducing tracing length. Other experts feel that the small details of CTG tracings are better evaluated using higher papers speeds. The vertical scale used for registration and viewing may also be different, and available alternatives are 20 or 30 bpm/cm. The paper scales used in each centre should be the one with which healthcare professionals are most familiar, because tracing interpretation depends on pattern recognition and these patterns may appear very different. Inadvertent use of paper scales to which the staff is unaccustomed may lead to erroneous interpretations of CTG features. For example, at 3 cm/min variability appears reduced to a clinician familiar with the 1 cm/min scale, while it may appear exaggerated in the opposite situation (see examples below). External versus internal FHR monitoring External FHR monitoring uses a Doppler ultrasound transducer to detect the movement of cardiac structures. The resulting signal requires signal modulation and autocorrelation to provide adequate quality recordings 8. This process results is an approximation of the true heart rate intervals, but this is considered to be sufficiently accurate for analysis. External FHR monitoring is more prone to signal loss, to inadvertent monitoring of the maternal heart rate 9 (Fig. 1), and to signal artefacts such as double-counting (Fig. 2) and half-counting 8, particularly during the second stage of labour. It may also not record fetal cardiac arrhythmias accurately. 5 BASELINE – this is the mean level of the most horizontal and less oscillatory FHR segments. It is estimated in time periods of 10 minutes and expressed in beats per minute (bpm). The baseline value may vary between subsequent 10-minute sections. In tracings with unstable FHR signals, review of previous segments and/or evaluation of longer time periods may be necessary to estimate the baseline 16, in particular during the 2nd stage of labour and to identify the fetal behavioural state of active wakefulness (see below – Fig. 3) that can lead to an erroneously high baseline estimation. Fig 3. Fetal behavioural state of active wakefulness. This pattern may lead to an erroneously high baseline estimation if it is identified at the top of accelerations. External FHR monitoring at 1 cm/min (top graph), 2 cm/min (middle graph) and 3 cm/min (bottom graph). Normal baseline – a value between 110 and 160 bpm. Preterm fetuses tend to have values towards the upper end of this range and post term fetuses towards the lower end. Some experts consider the normal baseline values at term to be between 110-150 bpm. Tachycardia – a baseline value above 160 bpm lasting more than 10 minutes. Maternal pyrexia is the most frequent cause of fetal tachycardia, and it may be of extra-uterine origin or associated with intrauterine infection. Epidural analgesia may also cause a rise in maternal temperature resulting in fetal tachycardia 17. In the initial stages of a non-acute fetal hypoxemia, catecholamine secretion may also result in tachycardia. Other less frequent causes are the administration of beta-agonist drugs 18 (salbutamol, terbutaline, ritodrine, fenoterol), parasympathetic blockers (atropine, escopolamine), and fetal arrhythmias such as supraventricular tachycardia and atrial flutter. Bradycardia – a baseline value below 110 bpm lasting more than 10 minutes Values between 100 and 110 bpm may occur in normal fetuses, especially in postdate pregnancies. Maternal hypothermia 19, administration of beta-blockers 20, and fetal arrhythmias such as atrial-ventricular block are other possible causes. VARIABILITY – refers to the oscillations in the FHR signal, evaluated as the average bandwidth amplitude of the signal in one-minute segments. Normal variability – a bandwidth amplitude of 5-25 bpm. 6 Reduced variability – a bandwidth amplitude below 5 bpm for more than 50 minutes in baseline segments 21 (Figs. 4-5), or for more than 3 minutes during decelerations 22 (Figs. 8-9). Reduced variability can occur due to central nervous system hypoxia/acidosis and resulting decreased sympathetic and parasympathetic activity, but it can also be due to previous cerebral injury 23, infection, administration of central nervous system depressants or parasympathetic blockers. During deep sleep, variability is usually in the lower range of normality, but the bandwidth amplitude is seldom under 5 bpm. There is a high degree of subjectivity in the visual evaluation of this parameter, and therefore careful re-evaluation is recommended in borderline situations. Following an initially normal CTG, reduced variability due to hypoxia is very unlikely to occur during labour without preceding or concomitant decelerations and a rise in the baseline. Fig 4. Reduced variability. External FHR monitoring at 1 cm/min (top graph), 2 cm/min (middle graph) and 3 cm/min (bottom graph). 7 Fig 5. Reduced variability – the baseline is affected by contractions causing decreases in FHR that are close to fulfilling the criteria for decelerations, but the bandwidth remains reduced. Internal FHR monitoring at 1 cm/min (top graph), 2 cm/min (middle graph) and 3 cm/min (bottom graph). Increased variability (saltatory pattern) – a bandwidth value exceeding 25 bpm lasting more than 30 minutes (Fig. 6). The pathophysiology of this pattern is incompletely understood, but it may be seen linked with recurrent decelerations, when hypoxia/acidosis evolves very rapidly. It is presumed to be caused by fetal autonomic instability/hyperactive autonomic system 24. Fig 6. Increased variability - saltatory pattern. Internal FHR monitoring at 1 cm/min (top graph), 2 cm/min (middle graph) and 3 cm/min (bottom graph). ACCELERATIONS – abrupt (onset to peak in less than 30 seconds) increases in FHR above the baseline, of more than 15 bpm in amplitude, and lasting more than 15 seconds but less than 10 minutes. Most accelerations coincide with fetal movements and are a sign of a neurologically responsive fetus that does not have hypoxia/acidosis. Before 32 weeks’ gestation, their amplitude and frequency may be lower (10 seconds and 10 bpm of amplitude). After 32-34 weeks, with the establishment of fetal behavioural states, accelerations rarely occur during periods of deep sleep, which can last up to 50 minutes 21. The absence of accelerations in an otherwise normal intrapartum CTG is of uncertain significance, but it is unlikely to indicate hypoxia/acidosis. Accelerations coinciding with uterine contractions, especially in the second stage of labour, suggest possible erroneous recording of the maternal heart rate, since the FHR more frequently decelerates with a contraction, while the maternal heart rate typically increases 9. 10 Fig 9. Prolonged deceleration. External FHR monitoring at 1 cm/min (top graph), 2 cm/min (middle graph) and 3 cm/min (bottom graph). SINUSOIDAL PATTERN – a regular, smooth, undulating signal, resembling a sine wave, with an amplitude of 5-15 bpm, and a frequency of 3-5 cycles per minute. This pattern lasts more than 30 minutes, and coincides with absent accelerations (Fig. 10). The pathophysiological basis of the sinusoidal pattern is incompletely understood, but it occurs in association with severe fetal anemia, as is found in anti-D allo-immunisation, fetal-maternal hemorrhage, twin-to-twin transfusion syndrome and ruptured vasa praevia. It has also been described in cases of acute fetal hypoxia, infection, cardiac malformations, hydrocephalus and gastroschisis 31. Fig 10. Sinusoidal pattern. External FHR monitoring at 1 cm/min (top graph), 2 cm/min (middle graph) and 3 cm/min (bottom graph). PSEUDO-SINUSOIDAL PATTERN – a pattern resembling the sinusoidal pattern, but with a more jagged “saw-tooth” appearance, rather than the smooth sine-wave form (Fig. 11). Its duration seldom exceeds 30 minutes and it is characterised by normal patterns before and after. This pattern has been described after analgesic administration to the mother, and during periods of fetal sucking and other mouth movements 32. It is sometimes difficult to distinguish the pseudo- sinusoidal pattern from the true sinusoidal pattern, leaving the short duration of the former as the most important variable to discriminate between the two. 11 Fig 11. Pseudo-sinusoidal pattern. External FHR monitoring at 1 cm/min (top graph), 2 cm/min (middle graph) and 3 cm/min (bottom graph). FETAL BEHAVIOURAL STATES – refers to periods of fetal quiescence reflecting deep sleep (no eye movements), alternating with periods of active sleep (rapid eye movements) and wakefulness 33,34. The occurrence of different behavioural states is a hallmark of fetal neurological responsiveness and absence of hypoxia/acidosis. Deep sleep can last up to 50 minutes 21 and is associated with a stable baseline, very rare accelerations, and borderline variability. Active sleep is the most frequent behavioural state, and is represented by a moderate number of accelerations and normal variability. Active wakefulness is rarer and represented by a large number of accelerations and normal variability (Fig. 1). In the latter pattern, accelerations may be so frequent as to cause difficulties in baseline estimation (see Fig 1 above). Transitions between the different patterns become clearer after 32-34 weeks of gestation, consequent to fetal nervous system maturation. CONTRACTIONS – these are bell-shaped gradual increases in the uterine activity signal followed by roughly symmetric decreases, with 45-120 seconds in total duration. Contractions are essential for the progression of labour, but they compress the vessels running inside the myometrium and may transiently decrease placental perfusion and/or cause umbilical cord compression (see Chapter 1). With the tocodynamometer, only the frequency of contractions can be reliably evaluated, but increased intensity and duration can also contribute to FHR changes. Tachysystole – represents an excessive frequency of contractions and is defined as the occurrence of more than 5 contractions in 10 minutes, in two successive 10-minute periods, or averaged over a 30-minute period. 5. TRACING CLASSIFICATION Tracing classification requires a previous evaluation of basic CTG features (see above). Tracings should be classified into one of three classes: normal, suspicious or pathological, according to the criteria presented in Table 1. Other classification systems including a larger number of tiers are recommended by some experts 35,36. Due to the changing nature of CTG signals during labour, re-evaluation of the tracing should be carried out at least every 30 minutes. 12 Normal Suspicious Pathological Baseline 110-160 bpm Lacking at least one characteristic of normality, but with no pathological features < 100 bpm Variability 5-25 bpm Reduced variability for > 50 min, increased variability for >30 min, or sinusoidal pattern for > 30 min Decelerations No repetitive* decelerations Repetitive* late or prolonged decelerations during > 30 min or 20 min if reduced variability, or one prolonged deceleration with > 5 min Interpretation Fetus with no hypoxia/acidosis Fetus with a low probability of having hypoxia/acidosis Fetus with a high probability of having hypoxia/acidosis Clinical Management No intervention necessary to improve fetal oxygenation state Action to correct reversible causes if identified, close monitoring or additional methods to evaluate fetal oxygenation (chapter 4). Immediate action to correct reversible causes, additional methods to evaluate fetal oxygenation (chapter 4), or if this is not possible expedite delivery. In acute situations (cord prolapse, uterine rupture or placental abruption) immediate delivery should be accomplished. Table 1. CTG classification criteria, interpretation and recommended management. The presence of accelerations denotes a fetus that does not have hypoxia/acidosis, but their absence during labour is of uncertain significance. *Decelerations are repetitive in nature when they are associated with more than 50% of uterine contractions 29. 6. CLINICAL DECISION Several factors, including gestational age and medication administered to the mother, can affect FHR features (see above), so CTG analysis needs to be integrated with other clinical information for a comprehensive interpretation and adequate management. As a general rule, if the fetus continues to maintain a stable baseline and a reassuring variability, the risk of hypoxia to the central organs is very unlikely. However, the general principles that should guide clinical management are outlined in Table 1. 7. ACTION IN SITUATIONS OF SUSPECTED FETAL HYPOXIA/ACIDOSIS When fetal hypoxia/acidosis is anticipated or suspected (suspicious and pathological tracings), and action is required to avoid adverse neonatal outcome, this does not necessarily mean an immediate cesarean section or instrumental vaginal delivery. The underlying cause for the appearance of the pattern can frequently be identified and the situation reversed, with subsequent recovery of adequate fetal oxygenation and the return to a normal tracing. Excessive uterine activity is the most frequent cause of fetal hypoxia/acidosis (see Chapter 1) and it can be detected by documenting tachysystole in the CTG tracing and/or palpating the uterine fundus. It can usually be reversed by reducing or stopping oxytocin infusion, removing administered prostaglandins if possible, and/or starting acute tocolysis with beta-adrenegic agonists (salbutamol, terbutaline, ritodrine) 37-39, atosiban 40, or nitroglycerine 41. During the second stage of labour, maternal pushing efforts can also contribute to fetal hypoxia/acidosis and the mother can be asked to stop pushing until the situation is reversed. Aorto-caval compression can occur in the supine position and lead to reduced placental perfusion. Excessive uterine activity may also be associated with the supine position 42,43, possibly due to the stimulation of the sacral plexus by the uterine weight. In these cases, turning the mother to her side is frequently followed by normalization of the CTG pattern. Transient cord compression is another common cause of CTG changes (variable decelerations), and these can sometimes be reverted by changing the maternal position or by performing amnioinfusion 44. Sudden maternal hypotension can also occur during labour, usually after epidural or spinal analgesia 45, and it is usually reversible by rapid fluid administration and/or an intravenous