J. Perinat. Med. 2014; aop
Malin Holzmann*, Stina Wretler, Sven Cnattingius and Lennart Nordström
Cardiotocography patterns and risk of intrapartum fetal acidemia Keywords: Cardiotocography (CTG); fetal blood sampling (FBS); fetal distress; fetal monitoring; metabolic acidosis.
Abstract Aim: To identify cardiotocography (CTG) patterns associated with increased risk of intrapartum fetal acidemia. Methods: A prospective observational cohort study of 1070 women with fetal scalp blood sampling (FBS) during labor was conducted at Karolinska University Hospital, Stockholm, Sweden. Women with a nonreassuring CTG pattern underwent FBS, and lactate concentration was measured at the bedside. Lactate concentrations > 4.8 mmol/L were defined as fetal acidemia. A senior obstetrician, blinded to the lactate concentration at FBS, visually interpreted the CTG tracings that had prompted FBS. Results: There were 2134 FBSs performed on 1070 laboring women, constituting 11% of all deliveries at this labor ward. The CTG patterns with the highest frequency of lactacidemia at FBS were late or severe variable decelerations combined with tachycardia (20%–25% at first FBS and 33%–49% at last FBS). With a normal baseline fetal heart rate, normal variability, and absence of serious decelerations, the fetal scalp blood lactate concentration at the first FBS was normal in 97.5% of cases. The group with isolated reduced variability had no increased prevalence of acidemia and median lactate concentration did not differ from the normal group. Conclusion: Isolated reduced variability is in most cases not a sign of hypoxia. If development of hypoxia is ruled out with one FBS, this pattern does not require monitoring with repetitive FBSs throughout labor. Late decelerations and severe variable decelerations increase the risk for intrapartum fetal metabolic acidemia to the same extent. The combination of these decelerations and tachycardia was associated with the highest rate of fetal metabolic acidemia.
*Corresponding author: Malin Holzmann, Department of Obstetrics and Gynecology, Karolinska University Hospital, 171 76 Stockholm, Sweden, Tel.: +46 8 517 70 000, E-mail: [email protected] Malin Holzmann, Stina Wretler and Lennart Nordström: Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden Sven Cnattingius: Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden
DOI 10.1515/jpm-2014-0105 Received March 30, 2014. Accepted May 13, 2014.
Introduction The primary goal of intrapartum fetal surveillance is to identify fetuses with developing hypoxia to enable timely delivery before tissue injury has occurred. Fetal monitoring with cardiotocography (CTG) has high sensitivity, but poor specificity [1, 18]. A secondary goal of intrapartum fetal surveillance is to avoid unnecessary interventions, which may increase the risk of maternal morbidity. Fetal blood sampling (FBS) is a complementary method used when CTG traces are nonreassuring, as a decreased pH, alternatively increased lactate concentration, in fetal scalp blood identifies the development of acidemia [13, 34]. FBS is also a reliable method to exclude fetal hypoxia, as false-negative tests are unlikely [34]. If FBS confirms evolving fetal acidemia it is possible for the obstetrician to take timely action to prevent birth asphyxia [5, 10]. The wide introduction of CTG into clinical practice preceded studies concerning the pathophysiological meaning of the parameters assessed in CTG, and guidelines are more the opinion of experts than fully evidencebased [12, 15–17]. Therefore, guidelines for FBS are not completely evidence-based either. Common causes of concern during labor are disappearance of fetal heart rate (FHR) accelerations, isolated reduced variability, and simple variable decelerations with large amplitude, all of uncertain value concerning the risk of developing fetal acidemia. Earlier studies correlating different CTG abnormalities to fetal status had small study populations [3, 6, 14], or used neonatal outcome measures, e.g., umbilical blood gases and cerebral palsy as outcomes [18, 35]. Umbilical blood gases are influenced by the action taken and time interval to delivery and intrapartum acidemia is only a minor contribution to cerebral palsy.
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2 Holzmann et al., Cardiotocography patterns and intrapartum acidemia
The aim of this study was to investigate the association between different CTG patterns and intrapartum fetal metabolic acidemia. We hypothesized that occurrence of decelerations in combination with decreased variability and/or tachycardia has stronger association with acidemia than decelerations with normal baseline and variability.
Half of the women had more than one FBS. We, therefore, present results for both the first sampling, including the total population, and the last sampling, excluding cases with active pushing prior to sampling, as active pushing is known to increase the lactate concentration [20].
Statistics
Methods This is a prospective observational cohort study of women who underwent FBS due to a nonreassuring CTG trace during labor at Karolinska University Hospital, Stockholm, Sweden from February 2009 to February 2011. Inclusion criteria were simplex pregnancy, ≥ 34 weeks of gestation, cephalic presentation, and indication for FBS according to the attending doctor. The study was approved by the Regional Ethics Committee of Stockholm (2008/1618-31, 2011/478-32). Intrapartum fetal surveillance with CTG was performed according to Swedish guidelines [19], and summarized as follows: all women had an admission CTG; with a normal test and the woman was considered at low risk, intermittent CTG monitoring every 2 h was recommended. Women considered to be at high risk, having epidural analgesia or oxytocin augmentation had continuous CTG monitoring. CTG interpretation followed the guidelines of the Swedish Society of Obstetrics and Gynecology (SFOG) [30], based on the international classification system of the International Federation of Gynecology and Obstetrics (FIGO) [12]. The attending physician decided upon FBS if the CTG trace was visually interpreted as nonreassuring. FBS was performed according to clinical routine; 5 μL of fetal scalp blood was collected after wiping dry from amniotic fluid and applying silicone gel. Analysis was done at the bedside using Lactate Pro™ (KDK Corp., Kyoto, Japan), calibrated every 50th analysis. The coefficient of variance has been shown to be ≤ 4% in the range 2.1–5.3 mmol/L [21]. Action was taken according to clinical guidelines: lactate < 4.2 mmol/L = normal, continue labor; lactate 4.2–4.8 mmol/L = preacidemia, repeated FBS within 20–30 min; and lactate > 4.8 mmol/L = acidemia, consider delivery [13]. A senior obstetrician (LN), blinded to the lactate concentration at sampling, interpreted all CTG tracings with focus on the last 60 min prior to each FBS. We documented baseline FHR, variability, accelerations, type of decelerations, and duration of CTG pattern prior to FBS. Definitions published by FIGO were used, i.e., FHR (normal) 110–150 beats per minute (bpm), bradycardia < 110 bpm, and tachycardia > 150 bpm. Variability: normal 5–25 bpm, reduced: 2–4 bpm, absent: < 2 bpm, and increased: > 25 bpm, accelerations: transient increase in FHR of ≥ 15 bpm for ≥ 15 s, and decelerations: transient episodes of slowing of FHR below baseline level of ≥ 15 bpm lasting ≥ 15 s [12]. Severe variable decelerations were defined as having a variable shape, an abrupt fall from baseline FHR to nadir of deceleration, and a duration > 60 s. Late decelerations were defined as start of deceleration after a peak of contraction, uniform shape, and gradual fall to nadir of deceleration. We defined a bradycardic episode as baseline FHR < 110 bpm for > 3 min occurring within 30 min before sampling, including prolonged decelerations lasting < 10 min and bradycardia for > 10 min. Simple variable decelerations (duration < 60 s) and early decelerations (starting before peak of contraction) were referred to the normal group.
We made a power calculation based on an interim analysis of 176 cases. To detect a difference in the frequency of lactate concentration > 4.8 mmol/L between 5%, as estimated for the normal group, and 15%, with a power of 80%, 940 cases would be required, and 327 cases for a difference between 5% and 25%. Chi-square test and Fisher’s exact test were used for comparison of frequencies. A P-value < 0.05 was considered significant. Due to a skewed distribution of several continuous variables, data are presented as medians, and the Mann-Whitney U-test was used for comparison between groups. Statistica 11 (Statsoft Inc., Tulsa, OK, USA) software was used for all statistical analyses.
Results During the study period, there were 2134 FBSs performed on 1070 women; 48% had one FBS and the median was two samplings (range 1–8). Sixty-eight percent had their first FBS during first stage of labor from a cervical dilation of 2 cm, and 92% had internal CTG monitoring. Characteristics of the study population are shown in Table 1. The blinded reviewer (LN) interpreted the CTG pattern prior to the first FBS as having a normal baseline and variability without serious decelerations in nearly 23% of cases. There were simple variable or early decelerations in 75%, and absence of accelerations in half of these cases. The indication for FBS according to the attending physician had been either another interpretation of Table 1 Characteristics of study population [medians (range) and numbers (%)].
Total population (n = 1070)
Maternal age (years) Gestational age (weeks+days) Nulliparous n (%) Intrapartum fever n (%) Thick meconium n (%) Oxytocin augmentation prior to FBS n (%) Delivery mode n (%) Spontaneous Ventouse Cesarean Birth weight (g)
31a (15–47b) 40+3a (34+1–42+4) 771 (72.1) 179 (16.7) 75 (7.0) 652 (60.9)
a
median, brange.
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421 (39.4) 349 (32.6) 300 (28.0) 3501a (1638–5340b)
Holzmann et al., Cardiotocography patterns and intrapartum acidemia 3
decelerations or variability, or absence of accelerations in these cases. Numbers and rates of CTG patterns are shown in Table 2. Reduced variability, tachycardia and the combination of the two, implied FBS in 12%–14%. Severe variable decelerations were twice as common as late decelerations, 12% vs. 5%. Decelerations with tachycardia and/or reduced variability existed in approximately 3% of cases. At the first FBS, cases with normal baseline and variability without serious decelerations had normal lactate concentrations in 97.5%, and isolated reduced variability was associated with a similar high proportion of normal lactate concentrations (Table 2). The median lactate concentrations between the two groups did not differ (Table 3). Within the group with reduced variability, the absence of accelerations for more than 60 min did not significantly increase the proportion of acidemia at FBS [4.0% (CI 95% 1.3%–6.7%)]. Cases with tachycardia did not have a higher median lactate concentration than cases with normal baseline FHR, unless the tachycardia was accompanied by serious decelerations (Table 3). The CTG patterns with the highest frequency of lactate concentration > 4.8 mmol/L at FBS were severe variable or late decelerations in combination with tachycardia (25% and 20%, respectively) (Table 2). The median lactate concentrations were in these cases 1.6 and 0.9 mmol/L higher than in the reference group, respectively (Table 3). If cases with maternal fever ( > 38.0°C) were excluded in cases with tachycardia the proportion of lactacidemia did not change (data shown upon request). At the last FBS, the rate of increased lactate concentration was 4.8% in the group with normal baseline and
variability, and 22% if either late or severe variable decelerations occurred (Table 4). The proportion of acidemia was further increased if either of these decelerations occurred together with reduced variability (29%) or with tachycardia (33% and 49%, respectively). The median lactate concentration was nearly doubled in cases with tachycardia combined with serious decelerations (Table 5). There were 148 cases with acceleration as a response to FBS, and two of these had lactacidemia at sampling. Among cases with no FHR reaction to FBS, 76/668 had acidemia (data shown upon request). Fifteen neonates had an Apgar score < 7 at 5 min. Nine had umbilical artery pH (UA-pH) < 7.00, and 14 had metabolic acidemia (UA-pH < 7.05 and base deficit, BDblood > 12 mmol/L). These cases were evenly distributed in the groups with different CTG abnormalities. One neonate had hypoxic ischemic encephalopathy (HIE).
Comment A CTG tracing with isolated reduced variability was not associated with a higher lactate concentration or increased proportion of fetal acidemia compared with a normal baseline FHR and variability. Cases with severe variable decelerations and late decelerations had similar median lactate concentration and proportions of fetal lactacidemia at FBS. Cases with tachycardia and late or severe variable decelerations had the highest frequency of fetal metabolic acidemia, and at the last FBS, the median lactate concentration at FBS was nearly doubled in these cases compared with the “normal” group.
Table 2 Proportions of fetal lactacidemia at first FBS in groups with different CTG patterns.
Total numbers (%)
Numbers with lactate > 4.8 mmol/L
% (95% CI)
P-valuea
Normal baseline and variability Reduced variability Absent variability Increased variability Bradycardic episode Tachycardia Tachycardia+reduced variability Severe variable decelerations Late decelerations Severe variable decelerations+reduced variability Late decelerations+reduced variability Severe variable decelerations+tachycardia Late decelerations+tachycardia Missing+undefinable pattern Total
242 (22.6) 154 (14.4) 32 (3.0) 10 (0.9) 46 (4.3) 124 (11.6) 149 (13.9) 127 (11.9) 58 (5.4) 28 (2.6) 25 (2.3) 32 (3.0) 30 (2.8) 13 (1.2) 1070
6 4 4 2 10 10 9 18 8 4 3 8 6 2 94
2.5 (0.1–4.5) 2.6 (0.1–5.1) 12.5 (0.4–24.6) 20.0 (0–50.2) 21.7 (9.4–34.1) 8.1 (3.2–12.9) 6.0 (2.2–9.9) 14.2 (8.0–20.3) 13.8 (4.6–22.9) 14.3 (0.5–28.1) 12.0 (0–25.7) 25.0 (9.1–40.9) 20.0 (4.8–35.2) 15.4 8.8
1.0 0.020 0.035 < 0.001 0.027 0.102 < 0.001 0.001 0.013 0.042 < 0.001 0.001 0.057
CTG-pattern
a
P-value calculated with the two-tailed Fisher’s exact test in comparison to normal CTG.
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4 Holzmann et al., Cardiotocography patterns and intrapartum acidemia Table 3 Median of lactate concentration at first FBS in groups with different CTG patterns. CTG-pattern
Median (mmol/L)
Normal baseline and variability (242) Reduced variability (154) Absent variability (32) Increased variability (10) Bradycardic episode (46) Tachycardia (124) Tachycardia+reduced variability (149) Severe variable decelerations (127) Late decelerations (58) Severe variable decelerations+reduced variability (28) Late decelerations+reduced variability (25) Severe variable decelerations+tachycardia (32) Late decelerations+tachycardia (30) Missing+undefinable pattern Total
2.2 2.15 2.35 3.4 3.15 2.4 2.4 3.2 3.2 3.1 3.2 3.8 3.1 3.2 2.6
25th–75th percentile
P-valuea
1.8–3.1 1.7–2.6 1.9–3.2 2.6–4.1 2.2–4.4 2.0–3.4 1.9–3.3 2.3–4.2 2.2–4.1 2.2–4.1 2.7–4.1 3.1–4.8 2.4–4.7 1.4–5.3 2.0–3.4
0.0176 0.833 0.008 < 0.001 0.0125 0.223 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 0.478
a
P-value calculated using the Mann-Whitney test comparison to normal baseline and variability.
To our knowledge, there are few studies on the correlation between intrapartum CTG abnormalities and acid-base status in fetal scalp blood [3, 6, 14, 27]. The study populations ranged between 85 and 279 women. They were performed during the late 1960s to the early 1980s, when the understanding of CTG patterns was relatively new, definitions were different from guidelines used today, and in addition they measured pH in fetal scalp blood, thus not being able to differentiate between the harmless respiratory acidemia and the potentially dangerous metabolic acidemia. The study by Beard et al. [3] did not further specify the variable decelerations as
simple or severe/complicated. Other studies have used neonatal outcome measures. Decreased variability was associated with an increased risk for acidemia in umbilical artery [35], and cerebral palsy [18], but the former study did not differ between reduced and absent variability, and the latter also pointed at a false positivity rate of 99.8%. Saling showed that the use of CTG alone had low reliability in diagnosing hypoxia, and that suspicious or pathological heart rate patterns are accompanied by fetal preacidosis or acidosis in about 30% of cases [27], and similar results were presented by Palo and Erkkola [23].
Table 4 Proportions of fetal lactacidemia at last FBS in groups with different CTG patterns (cases with active pushing prior to sampling excluded). CTG-pattern
Total numbersa (%)
Numbers with lactate > 4.8 mmol/L
Normal baseline and variability Reduced variability Absent variability Increased variability Bradycardic episode Tachycardia Tachycardia+reduced variability Severe variable decelerations Late decelerations Severe variable decelerations+reduced variability Late decelerations+reduced variability Severe variable decelerations+tachycardia Late decelerations+tachycardia Missing+undefinable pattern Total
187 (21.1) 113 (12.7) 32 (3.6) 7 (0.8) 36 (4.1) 106 (11.9) 128 (14.4) 97 (10.9) 49 (5.5) 28 (3.2) 34 (3.8) 33 (3.7) 30 (3.4) 8 (0.9) 888
9 5 7 2 12 16 7 21 11 8 10 16 10 2 136
a
% (95% CI)
4.8 (1.7–7.9) 4.4 (0.6–8.3) 21.9 (6.7–37.1) 28.6 (0–73.7) 33.3 (17.2–49.5) 15.1 (8.2–22.0) 5.5 (1.5–9.5) 21.6 (13.3–30.0) 22.4 (10.3–34.6) 28.6 (10.7–46.4) 29.4 (13.3–45.5) 48.5 (30.5–66.5) 33.3 (15.4–51.2) 25.0 15.3
P-valueb
1.0 0.003 0.053 < 0.001 0.004 0.800 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 0.067
Cases with active pushing prior to sampling excluded. bP-value calculated with the two-tailed Fisher’s exact test in comparison to normal CTG.
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Holzmann et al., Cardiotocography patterns and intrapartum acidemia 5
Table 5 Median of lactate concentration at last FBS in groups with different CTG patterns. CTG-pattern (n)
Median (mmol/L)
Normal baseline and variability (187) Reduced variability (113) Absent variability (32) Increased variability (7) Bradycardic episode (36) Tachycardia(106) Tachycardia+reduced variability (128) Severe variable decelerations (96) Late decelerations (49) Severe variable decelerations+reduced variability (28) Late decelerations+reduced variability (34) Severe variable decelerations+tachycardia (33) Late decelerations+tachycardia (30) Missing+undefinable pattern (11) Total (888)
2.3 2.3 2.6 3.1 3.3 3.0 2.5 3.4 3.2 3.8 4.5 4.4 4.2 4.1 2.8
25th–75th percentile
P-valuea
1.9–3.2 1.8–2.9 1.8–4.4 2.1–5.7 2.7–5.2 2.2–4.0 2.0–3.3 2.4–4.4 2.4–4.6 2.5–5.0 3.2–5.0 3.3–5.4 3.1–5.1 3.8–6.1 2.1–4.0
0.20 0.373 0.077 < 0.001 < 0.001 0.204 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 0.013
Cases with active pushing prior to sampling excluded. aP-value calculated using the Mann-Whitney test comparison to normal baseline and variability.
We, therefore, found it relevant to perform a study with current guidelines for CTG interpretation and a measure of the metabolic component of fetal acid-base status. The use of FBS in 11% of all deliveries can be perceived as liberal, but is comparable to other obstetric units where FBS is a part of intrapartum fetal surveillance routine [8, 9, 32]. Isolated reduced variability was not associated with fetal metabolic acidemia in our study. One cautious interpretation of this finding is that it is sufficient to exclude evolving acidemia with one FBS. However, as we found no differences between isolated reduced variability and normal CTG tracing with respect to fetal metabolic acidemia, it is questionable that isolated reduced variability should be regarded as a sign of ongoing hypoxia. Severe variable and late decelerations have different origins, and most associations with poor neonatal outcomes are shown with late decelerations [2, 18, 25]. Animal studies and case-control studies have concluded that late decelerations are associated with chronic and acute hypoxia and often correlated to a suboptimal function of the placenta. Variable decelerations are explained as resulting from compression of the umbilical cord, and there are several definitions of subtypes concerning length, depth, and shape [7]. We found that the proportions of lactacidemia at FBS were similar among CTG patterns with severe variable decelerations and late decelerations. The 5% frequency of increased lactate concentration in cases with normal baseline and variability at the last FBS can be perceived as somewhat disturbing as the
strength of CTG is considered to be as high sensitivity, i.e., low risk of false negativity. A study from Steer et al. showed a sensitivity of 80% in detecting a cord artery pH below 7.17 by CTG [29], and Vintzileos et al. reported a sensitivity of 97% in the detection of a cord artery pH below 7.15 [31]. In light of those studies, and considering the cut-off level for scalp blood lactate set well below levels predicting severe neonatal morbidity [13], we find the 93% sensitivity for lactacidemia in scalp blood reassuring. The high proportion of lactacidemia after a bradycardic episode can be expected, as all samples were taken within 30 min from start of bradycardia. Lactate is not transported away over the placenta as quickly as CO2 [26], but acidemia is reversible if the FHR is restored to baseline with normalization of CTG afterwards [11]. If FBS is delayed after recovery of the FHR, a normal result can be expected and operative delivery avoided. There were very few cases with increased variability and it is not possible to draw conclusions from the present study regarding this very rare pattern. Our finding that FHR acceleration at the time of FBS is a reassuring sign of a nonacidemic fetus is in accord with the previous studies [28]. However, the majority of fetuses does not react with a prompt acceleration at FBS. The strength of this study is the size and study design; a cohort of all consecutive FBSs during the study period. It is prospective and blinded, as the CTG reviewer (LN) was not aware of the FBS result at the time of interpretation of the CTG traces. The limitations are similar to most studies concerning CTG interpretation, with shortcomings in inter-observer agreement [22, 24, 33]. We believe that our efforts in
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6 Holzmann et al., Cardiotocography patterns and intrapartum acidemia
structuring the CTG interpretation have minimized this weakness. Our finding that the two different types of serious decelerations have the same importance for fetal metabolic acidemia might even reduce future observer disagreement regarding decisions about intervention. Another limitation is that we did not take the duration of different CTG patterns into account. We believe it is unlikely that further subdivision of groups by duration would influence our results, but only make it more difficult to apply to clinical practice. We have also considered the possibility of selection bias. Some CTG patterns are more likely to indicate immediate delivery without preceded FBS, like persistent bradycardia or absent variability. In these groups the true proportion of lactacidemia is probably higher than in our study. We find it unlikely that a CTG tracing with isolated reduced variability would cause a decision upon immediate delivery. We, therefore, believe that our finding concerning isolated reduced variability can be regarded as reliable. Several CTG scoring systems have been evaluated and proposed. Although the high negative predictive value can provide a strong reassurance for fetal health, the CTG scores are not proven as predictable for defining fetal disease [4], and, therefore, we chose not to present our data in a scoring manner. We did not correlate lactate concentration in fetal blood with neonatal outcomes, as this was not the objective of the study. Actions taken due to CTG findings and FBS results make even short-term neonatal outcome measures such as HIE and UA-pH < 7.00 rare, demanding a larger sample size. Earlier studies have shown good correlations between fetal scalp blood lactate and neonatal outcomes, and the cut-off value for recommendation of intervention has been set well below values predicting low UA-pH and HIE [8, 13]. This is crucial for a diagnostic test as the most important issue must be to have no false-negative tests, i.e., no lactate concentration in normal range and the baby born with metabolic acidosis. As an increased lactate concentration in fetal scalp blood is an early marker in the hypoxic process, the analysis makes birth acidemia largely preventable if proper action is taken [10]. However, intrapartum diagnosis of fetal metabolic acidemia cannot prevent birth acidemia related to chronic fetal hypoxia, where damage might have already occurred before admission to the labor ward, or in obstetric emergencies, such as cord prolapse, placental abruption, or uterine rupture.
Conclusion Isolated reduced variability is not associated with increased rate of fetal acidemia, and this CTG pattern does
not require repeated FBS throughout labor. Severe variable decelerations and late decelerations correlate equally with fetal acidemia. Acknowledgments: We acknowledge the late professor Ingemar Ingemarsson for his valuable input regarding division of CTG patterns.
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[15] Liston R, Sawchuck D, Young D, Society of Obstetrics and Gynaecologists of Canada, British Columbia Perinatal Health Program. Fetal health surveillance: antepartum and intrapartum consensus guideline. J Obstet Gynaecol Can. 2007;29:S3–56. [16] Macones GA, Hankins GD, Spong CY, Hauth J, Moore T. The 2008 National Institute of Child Health and Human Development workshop report on electronic fetal monitoring: update on definitions, interpretation, and research guidelines. Obstet Gynecol. 2008;112:661–6. [17] National Institute for Clinical Excellence. Intrapartum care: care of healthy women and their babies during childbirth. Manchester: National Institute for Health and Clinical Excellence; 2007. [18] Nelson KB, Dambrosia JM, Ting TY, Grether JK. Uncertain value of electronic fetal monitoring in predicting cerebral palsy. N Engl J Med. 1996;334:613–8. [19] Nordström L, Waldenström U. Handläggning av normal förlossning. In: Welfare TNBoHa, editor. Stockholm: Socialstyrelsen; 2001. p. 69. [20] Nordstrom L, Achanna S, Naka K, Arulkumaran S. Fetal and maternal lactate increase during active second stage of labour. BJOG. 2001;108:263–8. [21] Nordstrom L, Chua S, Roy A, Arulkumaran S. Quality assessment of two lactate test strip methods suitable for obstetric use. J Perinat Med. 1998;26:83–8. [22] Ojala K, Makikallio K, Haapsamo M, Ijas H, Tekay A. Interobserver agreement in the assessment of intrapartum automated fetal electrocardiography in singleton pregnancies. Acta Obstet Gynecol Scand. 2008;87:536–40. [23] Palo P, Erkkola R. Intrapartal cardiotocography in prediction of well-being of small for gestational age newborns. Gynecol Obstet Invest. 1991;31:86–9. [24] Palomaki O, Luukkaala T, Luoto R, Tuimala R. Intrapartum cardiotocography – the dilemma of interpretational variation. J Perinat Med. 2006;34:298–302. [25] Parer JT, Krueger TR, Harris JL. Fetal oxygen consumption and mechanisms of heart rate response during artificially produced late decelerations of fetal heart rate in sheep. Am J Obstet Gynecol. 1980;136:478–82.
[26] Rooth G. Perinatal acid-base balance. Lund: Studentlitteratur; 1988. [27] Saling E. The measurement of fetal heart-rate and acid-base balance. 2nd Europ Cong Perinat Med. London: Karger; 1971. [28] Skupski DW, Eglinton GS. Intrapartum fetal stimulation tests: a meta-analysis. Obstet Gynecol. 2002;100:830. [29] Steer PJ, Eigbe F, Lissauer TJ, Beard RW. Interrelationships among abnormal cardiotocograms in labor, meconium staining of the amniotic fluid, arterial cord blood pH, and Apgar scores. Obstet Gynecol. 1989;74:715–21. [30] Swedish Society of Obstetrics and Gynecology. Guidelines for CTG interpretation and intervention. https://www.sfog.se/ media/17094/ctg_kort_slutversion.pdf. https://www.sfog.se/ start/rad-riktlinjer/sfog-rad-obstetrik/forlossning/: Swedish Society of Obstetrics and Gynecology; 2009. [31] Vintzileos AM, Nochimson DJ, Antsaklis A, Varvarigos I, Guzman ER, Knuppel RA. Comparison of intrapartum electronic fetal heart rate monitoring versus intermittent auscultation in detecting fetal acidemia at birth. Am J Obstet Gynecol. 1995;173:1021–4. [32] Westerhuis ME, Strasser SM, Moons KG, Mol BW, Visser GH, Kwee A. [Intrapartum foetal monitoring: from stethoscope to ST analysis of the ECG]. Nederlands Tijdschrift Voor Geneeskunde. 2009;153:B259. [33] Westerhuis ME, van Horen E, Kwee A, van der Tweel I, Visser GH, Moons KG. Inter- and intra-observer agreement of intrapartum ST analysis of the fetal electrocardiogram in women monitored by STAN. BJOG. 2009;16:545–51. [34] Wiberg-Itzel E, Lipponer C, Norman M, Herbst A, Prebensen D, Hansson A, et al. Determination of pH or lactate in fetal scalp blood in management of intrapartum fetal distress: randomised controlled multicentre trial. Br Med J. 2008;336:1284–7. [35] Williams KP, Galerneau F. Intrapartum fetal heart rate patterns in the prediction of neonatal acidemia. Am J Obstet Gynecol. 2003;188:820–3. The authors stated that there are no conflicts of interest regarding the publication of this article.
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Malin Holzmann*, Stina Wretler, Sven Cnattingius and Lennart Nordström
Cardiotocography patterns and risk of intrapartum fetal acidemia Keywords: Cardiotocography (CTG); fetal blood sampling (FBS); fetal distress; fetal monitoring; metabolic acidosis.
Abstract Aim: To identify cardiotocography (CTG) patterns associated with increased risk of intrapartum fetal acidemia. Methods: A prospective observational cohort study of 1070 women with fetal scalp blood sampling (FBS) during labor was conducted at Karolinska University Hospital, Stockholm, Sweden. Women with a nonreassuring CTG pattern underwent FBS, and lactate concentration was measured at the bedside. Lactate concentrations > 4.8 mmol/L were defined as fetal acidemia. A senior obstetrician, blinded to the lactate concentration at FBS, visually interpreted the CTG tracings that had prompted FBS. Results: There were 2134 FBSs performed on 1070 laboring women, constituting 11% of all deliveries at this labor ward. The CTG patterns with the highest frequency of lactacidemia at FBS were late or severe variable decelerations combined with tachycardia (20%–25% at first FBS and 33%–49% at last FBS). With a normal baseline fetal heart rate, normal variability, and absence of serious decelerations, the fetal scalp blood lactate concentration at the first FBS was normal in 97.5% of cases. The group with isolated reduced variability had no increased prevalence of acidemia and median lactate concentration did not differ from the normal group. Conclusion: Isolated reduced variability is in most cases not a sign of hypoxia. If development of hypoxia is ruled out with one FBS, this pattern does not require monitoring with repetitive FBSs throughout labor. Late decelerations and severe variable decelerations increase the risk for intrapartum fetal metabolic acidemia to the same extent. The combination of these decelerations and tachycardia was associated with the highest rate of fetal metabolic acidemia.
*Corresponding author: Malin Holzmann, Department of Obstetrics and Gynecology, Karolinska University Hospital, 171 76 Stockholm, Sweden, Tel.: +46 8 517 70 000, E-mail: [email protected] Malin Holzmann, Stina Wretler and Lennart Nordström: Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden Sven Cnattingius: Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden
DOI 10.1515/jpm-2014-0105 Received March 30, 2014. Accepted May 13, 2014.
Introduction The primary goal of intrapartum fetal surveillance is to identify fetuses with developing hypoxia to enable timely delivery before tissue injury has occurred. Fetal monitoring with cardiotocography (CTG) has high sensitivity, but poor specificity [1, 18]. A secondary goal of intrapartum fetal surveillance is to avoid unnecessary interventions, which may increase the risk of maternal morbidity. Fetal blood sampling (FBS) is a complementary method used when CTG traces are nonreassuring, as a decreased pH, alternatively increased lactate concentration, in fetal scalp blood identifies the development of acidemia [13, 34]. FBS is also a reliable method to exclude fetal hypoxia, as false-negative tests are unlikely [34]. If FBS confirms evolving fetal acidemia it is possible for the obstetrician to take timely action to prevent birth asphyxia [5, 10]. The wide introduction of CTG into clinical practice preceded studies concerning the pathophysiological meaning of the parameters assessed in CTG, and guidelines are more the opinion of experts than fully evidencebased [12, 15–17]. Therefore, guidelines for FBS are not completely evidence-based either. Common causes of concern during labor are disappearance of fetal heart rate (FHR) accelerations, isolated reduced variability, and simple variable decelerations with large amplitude, all of uncertain value concerning the risk of developing fetal acidemia. Earlier studies correlating different CTG abnormalities to fetal status had small study populations [3, 6, 14], or used neonatal outcome measures, e.g., umbilical blood gases and cerebral palsy as outcomes [18, 35]. Umbilical blood gases are influenced by the action taken and time interval to delivery and intrapartum acidemia is only a minor contribution to cerebral palsy.
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2 Holzmann et al., Cardiotocography patterns and intrapartum acidemia
The aim of this study was to investigate the association between different CTG patterns and intrapartum fetal metabolic acidemia. We hypothesized that occurrence of decelerations in combination with decreased variability and/or tachycardia has stronger association with acidemia than decelerations with normal baseline and variability.
Half of the women had more than one FBS. We, therefore, present results for both the first sampling, including the total population, and the last sampling, excluding cases with active pushing prior to sampling, as active pushing is known to increase the lactate concentration [20].
Statistics
Methods This is a prospective observational cohort study of women who underwent FBS due to a nonreassuring CTG trace during labor at Karolinska University Hospital, Stockholm, Sweden from February 2009 to February 2011. Inclusion criteria were simplex pregnancy, ≥ 34 weeks of gestation, cephalic presentation, and indication for FBS according to the attending doctor. The study was approved by the Regional Ethics Committee of Stockholm (2008/1618-31, 2011/478-32). Intrapartum fetal surveillance with CTG was performed according to Swedish guidelines [19], and summarized as follows: all women had an admission CTG; with a normal test and the woman was considered at low risk, intermittent CTG monitoring every 2 h was recommended. Women considered to be at high risk, having epidural analgesia or oxytocin augmentation had continuous CTG monitoring. CTG interpretation followed the guidelines of the Swedish Society of Obstetrics and Gynecology (SFOG) [30], based on the international classification system of the International Federation of Gynecology and Obstetrics (FIGO) [12]. The attending physician decided upon FBS if the CTG trace was visually interpreted as nonreassuring. FBS was performed according to clinical routine; 5 μL of fetal scalp blood was collected after wiping dry from amniotic fluid and applying silicone gel. Analysis was done at the bedside using Lactate Pro™ (KDK Corp., Kyoto, Japan), calibrated every 50th analysis. The coefficient of variance has been shown to be ≤ 4% in the range 2.1–5.3 mmol/L [21]. Action was taken according to clinical guidelines: lactate < 4.2 mmol/L = normal, continue labor; lactate 4.2–4.8 mmol/L = preacidemia, repeated FBS within 20–30 min; and lactate > 4.8 mmol/L = acidemia, consider delivery [13]. A senior obstetrician (LN), blinded to the lactate concentration at sampling, interpreted all CTG tracings with focus on the last 60 min prior to each FBS. We documented baseline FHR, variability, accelerations, type of decelerations, and duration of CTG pattern prior to FBS. Definitions published by FIGO were used, i.e., FHR (normal) 110–150 beats per minute (bpm), bradycardia < 110 bpm, and tachycardia > 150 bpm. Variability: normal 5–25 bpm, reduced: 2–4 bpm, absent: < 2 bpm, and increased: > 25 bpm, accelerations: transient increase in FHR of ≥ 15 bpm for ≥ 15 s, and decelerations: transient episodes of slowing of FHR below baseline level of ≥ 15 bpm lasting ≥ 15 s [12]. Severe variable decelerations were defined as having a variable shape, an abrupt fall from baseline FHR to nadir of deceleration, and a duration > 60 s. Late decelerations were defined as start of deceleration after a peak of contraction, uniform shape, and gradual fall to nadir of deceleration. We defined a bradycardic episode as baseline FHR < 110 bpm for > 3 min occurring within 30 min before sampling, including prolonged decelerations lasting < 10 min and bradycardia for > 10 min. Simple variable decelerations (duration < 60 s) and early decelerations (starting before peak of contraction) were referred to the normal group.
We made a power calculation based on an interim analysis of 176 cases. To detect a difference in the frequency of lactate concentration > 4.8 mmol/L between 5%, as estimated for the normal group, and 15%, with a power of 80%, 940 cases would be required, and 327 cases for a difference between 5% and 25%. Chi-square test and Fisher’s exact test were used for comparison of frequencies. A P-value < 0.05 was considered significant. Due to a skewed distribution of several continuous variables, data are presented as medians, and the Mann-Whitney U-test was used for comparison between groups. Statistica 11 (Statsoft Inc., Tulsa, OK, USA) software was used for all statistical analyses.
Results During the study period, there were 2134 FBSs performed on 1070 women; 48% had one FBS and the median was two samplings (range 1–8). Sixty-eight percent had their first FBS during first stage of labor from a cervical dilation of 2 cm, and 92% had internal CTG monitoring. Characteristics of the study population are shown in Table 1. The blinded reviewer (LN) interpreted the CTG pattern prior to the first FBS as having a normal baseline and variability without serious decelerations in nearly 23% of cases. There were simple variable or early decelerations in 75%, and absence of accelerations in half of these cases. The indication for FBS according to the attending physician had been either another interpretation of Table 1 Characteristics of study population [medians (range) and numbers (%)].
Total population (n = 1070)
Maternal age (years) Gestational age (weeks+days) Nulliparous n (%) Intrapartum fever n (%) Thick meconium n (%) Oxytocin augmentation prior to FBS n (%) Delivery mode n (%) Spontaneous Ventouse Cesarean Birth weight (g)
31a (15–47b) 40+3a (34+1–42+4) 771 (72.1) 179 (16.7) 75 (7.0) 652 (60.9)
a
median, brange.
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421 (39.4) 349 (32.6) 300 (28.0) 3501a (1638–5340b)
Holzmann et al., Cardiotocography patterns and intrapartum acidemia 3
decelerations or variability, or absence of accelerations in these cases. Numbers and rates of CTG patterns are shown in Table 2. Reduced variability, tachycardia and the combination of the two, implied FBS in 12%–14%. Severe variable decelerations were twice as common as late decelerations, 12% vs. 5%. Decelerations with tachycardia and/or reduced variability existed in approximately 3% of cases. At the first FBS, cases with normal baseline and variability without serious decelerations had normal lactate concentrations in 97.5%, and isolated reduced variability was associated with a similar high proportion of normal lactate concentrations (Table 2). The median lactate concentrations between the two groups did not differ (Table 3). Within the group with reduced variability, the absence of accelerations for more than 60 min did not significantly increase the proportion of acidemia at FBS [4.0% (CI 95% 1.3%–6.7%)]. Cases with tachycardia did not have a higher median lactate concentration than cases with normal baseline FHR, unless the tachycardia was accompanied by serious decelerations (Table 3). The CTG patterns with the highest frequency of lactate concentration > 4.8 mmol/L at FBS were severe variable or late decelerations in combination with tachycardia (25% and 20%, respectively) (Table 2). The median lactate concentrations were in these cases 1.6 and 0.9 mmol/L higher than in the reference group, respectively (Table 3). If cases with maternal fever ( > 38.0°C) were excluded in cases with tachycardia the proportion of lactacidemia did not change (data shown upon request). At the last FBS, the rate of increased lactate concentration was 4.8% in the group with normal baseline and
variability, and 22% if either late or severe variable decelerations occurred (Table 4). The proportion of acidemia was further increased if either of these decelerations occurred together with reduced variability (29%) or with tachycardia (33% and 49%, respectively). The median lactate concentration was nearly doubled in cases with tachycardia combined with serious decelerations (Table 5). There were 148 cases with acceleration as a response to FBS, and two of these had lactacidemia at sampling. Among cases with no FHR reaction to FBS, 76/668 had acidemia (data shown upon request). Fifteen neonates had an Apgar score < 7 at 5 min. Nine had umbilical artery pH (UA-pH) < 7.00, and 14 had metabolic acidemia (UA-pH < 7.05 and base deficit, BDblood > 12 mmol/L). These cases were evenly distributed in the groups with different CTG abnormalities. One neonate had hypoxic ischemic encephalopathy (HIE).
Comment A CTG tracing with isolated reduced variability was not associated with a higher lactate concentration or increased proportion of fetal acidemia compared with a normal baseline FHR and variability. Cases with severe variable decelerations and late decelerations had similar median lactate concentration and proportions of fetal lactacidemia at FBS. Cases with tachycardia and late or severe variable decelerations had the highest frequency of fetal metabolic acidemia, and at the last FBS, the median lactate concentration at FBS was nearly doubled in these cases compared with the “normal” group.
Table 2 Proportions of fetal lactacidemia at first FBS in groups with different CTG patterns.
Total numbers (%)
Numbers with lactate > 4.8 mmol/L
% (95% CI)
P-valuea
Normal baseline and variability Reduced variability Absent variability Increased variability Bradycardic episode Tachycardia Tachycardia+reduced variability Severe variable decelerations Late decelerations Severe variable decelerations+reduced variability Late decelerations+reduced variability Severe variable decelerations+tachycardia Late decelerations+tachycardia Missing+undefinable pattern Total
242 (22.6) 154 (14.4) 32 (3.0) 10 (0.9) 46 (4.3) 124 (11.6) 149 (13.9) 127 (11.9) 58 (5.4) 28 (2.6) 25 (2.3) 32 (3.0) 30 (2.8) 13 (1.2) 1070
6 4 4 2 10 10 9 18 8 4 3 8 6 2 94
2.5 (0.1–4.5) 2.6 (0.1–5.1) 12.5 (0.4–24.6) 20.0 (0–50.2) 21.7 (9.4–34.1) 8.1 (3.2–12.9) 6.0 (2.2–9.9) 14.2 (8.0–20.3) 13.8 (4.6–22.9) 14.3 (0.5–28.1) 12.0 (0–25.7) 25.0 (9.1–40.9) 20.0 (4.8–35.2) 15.4 8.8
1.0 0.020 0.035 < 0.001 0.027 0.102 < 0.001 0.001 0.013 0.042 < 0.001 0.001 0.057
CTG-pattern
a
P-value calculated with the two-tailed Fisher’s exact test in comparison to normal CTG.
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4 Holzmann et al., Cardiotocography patterns and intrapartum acidemia Table 3 Median of lactate concentration at first FBS in groups with different CTG patterns. CTG-pattern
Median (mmol/L)
Normal baseline and variability (242) Reduced variability (154) Absent variability (32) Increased variability (10) Bradycardic episode (46) Tachycardia (124) Tachycardia+reduced variability (149) Severe variable decelerations (127) Late decelerations (58) Severe variable decelerations+reduced variability (28) Late decelerations+reduced variability (25) Severe variable decelerations+tachycardia (32) Late decelerations+tachycardia (30) Missing+undefinable pattern Total
2.2 2.15 2.35 3.4 3.15 2.4 2.4 3.2 3.2 3.1 3.2 3.8 3.1 3.2 2.6
25th–75th percentile
P-valuea
1.8–3.1 1.7–2.6 1.9–3.2 2.6–4.1 2.2–4.4 2.0–3.4 1.9–3.3 2.3–4.2 2.2–4.1 2.2–4.1 2.7–4.1 3.1–4.8 2.4–4.7 1.4–5.3 2.0–3.4
0.0176 0.833 0.008 < 0.001 0.0125 0.223 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 0.478
a
P-value calculated using the Mann-Whitney test comparison to normal baseline and variability.
To our knowledge, there are few studies on the correlation between intrapartum CTG abnormalities and acid-base status in fetal scalp blood [3, 6, 14, 27]. The study populations ranged between 85 and 279 women. They were performed during the late 1960s to the early 1980s, when the understanding of CTG patterns was relatively new, definitions were different from guidelines used today, and in addition they measured pH in fetal scalp blood, thus not being able to differentiate between the harmless respiratory acidemia and the potentially dangerous metabolic acidemia. The study by Beard et al. [3] did not further specify the variable decelerations as
simple or severe/complicated. Other studies have used neonatal outcome measures. Decreased variability was associated with an increased risk for acidemia in umbilical artery [35], and cerebral palsy [18], but the former study did not differ between reduced and absent variability, and the latter also pointed at a false positivity rate of 99.8%. Saling showed that the use of CTG alone had low reliability in diagnosing hypoxia, and that suspicious or pathological heart rate patterns are accompanied by fetal preacidosis or acidosis in about 30% of cases [27], and similar results were presented by Palo and Erkkola [23].
Table 4 Proportions of fetal lactacidemia at last FBS in groups with different CTG patterns (cases with active pushing prior to sampling excluded). CTG-pattern
Total numbersa (%)
Numbers with lactate > 4.8 mmol/L
Normal baseline and variability Reduced variability Absent variability Increased variability Bradycardic episode Tachycardia Tachycardia+reduced variability Severe variable decelerations Late decelerations Severe variable decelerations+reduced variability Late decelerations+reduced variability Severe variable decelerations+tachycardia Late decelerations+tachycardia Missing+undefinable pattern Total
187 (21.1) 113 (12.7) 32 (3.6) 7 (0.8) 36 (4.1) 106 (11.9) 128 (14.4) 97 (10.9) 49 (5.5) 28 (3.2) 34 (3.8) 33 (3.7) 30 (3.4) 8 (0.9) 888
9 5 7 2 12 16 7 21 11 8 10 16 10 2 136
a
% (95% CI)
4.8 (1.7–7.9) 4.4 (0.6–8.3) 21.9 (6.7–37.1) 28.6 (0–73.7) 33.3 (17.2–49.5) 15.1 (8.2–22.0) 5.5 (1.5–9.5) 21.6 (13.3–30.0) 22.4 (10.3–34.6) 28.6 (10.7–46.4) 29.4 (13.3–45.5) 48.5 (30.5–66.5) 33.3 (15.4–51.2) 25.0 15.3
P-valueb
1.0 0.003 0.053 < 0.001 0.004 0.800 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 0.067
Cases with active pushing prior to sampling excluded. bP-value calculated with the two-tailed Fisher’s exact test in comparison to normal CTG.
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Holzmann et al., Cardiotocography patterns and intrapartum acidemia 5
Table 5 Median of lactate concentration at last FBS in groups with different CTG patterns. CTG-pattern (n)
Median (mmol/L)
Normal baseline and variability (187) Reduced variability (113) Absent variability (32) Increased variability (7) Bradycardic episode (36) Tachycardia(106) Tachycardia+reduced variability (128) Severe variable decelerations (96) Late decelerations (49) Severe variable decelerations+reduced variability (28) Late decelerations+reduced variability (34) Severe variable decelerations+tachycardia (33) Late decelerations+tachycardia (30) Missing+undefinable pattern (11) Total (888)
2.3 2.3 2.6 3.1 3.3 3.0 2.5 3.4 3.2 3.8 4.5 4.4 4.2 4.1 2.8
25th–75th percentile
P-valuea
1.9–3.2 1.8–2.9 1.8–4.4 2.1–5.7 2.7–5.2 2.2–4.0 2.0–3.3 2.4–4.4 2.4–4.6 2.5–5.0 3.2–5.0 3.3–5.4 3.1–5.1 3.8–6.1 2.1–4.0
0.20 0.373 0.077 < 0.001 < 0.001 0.204 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 0.013
Cases with active pushing prior to sampling excluded. aP-value calculated using the Mann-Whitney test comparison to normal baseline and variability.
We, therefore, found it relevant to perform a study with current guidelines for CTG interpretation and a measure of the metabolic component of fetal acid-base status. The use of FBS in 11% of all deliveries can be perceived as liberal, but is comparable to other obstetric units where FBS is a part of intrapartum fetal surveillance routine [8, 9, 32]. Isolated reduced variability was not associated with fetal metabolic acidemia in our study. One cautious interpretation of this finding is that it is sufficient to exclude evolving acidemia with one FBS. However, as we found no differences between isolated reduced variability and normal CTG tracing with respect to fetal metabolic acidemia, it is questionable that isolated reduced variability should be regarded as a sign of ongoing hypoxia. Severe variable and late decelerations have different origins, and most associations with poor neonatal outcomes are shown with late decelerations [2, 18, 25]. Animal studies and case-control studies have concluded that late decelerations are associated with chronic and acute hypoxia and often correlated to a suboptimal function of the placenta. Variable decelerations are explained as resulting from compression of the umbilical cord, and there are several definitions of subtypes concerning length, depth, and shape [7]. We found that the proportions of lactacidemia at FBS were similar among CTG patterns with severe variable decelerations and late decelerations. The 5% frequency of increased lactate concentration in cases with normal baseline and variability at the last FBS can be perceived as somewhat disturbing as the
strength of CTG is considered to be as high sensitivity, i.e., low risk of false negativity. A study from Steer et al. showed a sensitivity of 80% in detecting a cord artery pH below 7.17 by CTG [29], and Vintzileos et al. reported a sensitivity of 97% in the detection of a cord artery pH below 7.15 [31]. In light of those studies, and considering the cut-off level for scalp blood lactate set well below levels predicting severe neonatal morbidity [13], we find the 93% sensitivity for lactacidemia in scalp blood reassuring. The high proportion of lactacidemia after a bradycardic episode can be expected, as all samples were taken within 30 min from start of bradycardia. Lactate is not transported away over the placenta as quickly as CO2 [26], but acidemia is reversible if the FHR is restored to baseline with normalization of CTG afterwards [11]. If FBS is delayed after recovery of the FHR, a normal result can be expected and operative delivery avoided. There were very few cases with increased variability and it is not possible to draw conclusions from the present study regarding this very rare pattern. Our finding that FHR acceleration at the time of FBS is a reassuring sign of a nonacidemic fetus is in accord with the previous studies [28]. However, the majority of fetuses does not react with a prompt acceleration at FBS. The strength of this study is the size and study design; a cohort of all consecutive FBSs during the study period. It is prospective and blinded, as the CTG reviewer (LN) was not aware of the FBS result at the time of interpretation of the CTG traces. The limitations are similar to most studies concerning CTG interpretation, with shortcomings in inter-observer agreement [22, 24, 33]. We believe that our efforts in
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6 Holzmann et al., Cardiotocography patterns and intrapartum acidemia
structuring the CTG interpretation have minimized this weakness. Our finding that the two different types of serious decelerations have the same importance for fetal metabolic acidemia might even reduce future observer disagreement regarding decisions about intervention. Another limitation is that we did not take the duration of different CTG patterns into account. We believe it is unlikely that further subdivision of groups by duration would influence our results, but only make it more difficult to apply to clinical practice. We have also considered the possibility of selection bias. Some CTG patterns are more likely to indicate immediate delivery without preceded FBS, like persistent bradycardia or absent variability. In these groups the true proportion of lactacidemia is probably higher than in our study. We find it unlikely that a CTG tracing with isolated reduced variability would cause a decision upon immediate delivery. We, therefore, believe that our finding concerning isolated reduced variability can be regarded as reliable. Several CTG scoring systems have been evaluated and proposed. Although the high negative predictive value can provide a strong reassurance for fetal health, the CTG scores are not proven as predictable for defining fetal disease [4], and, therefore, we chose not to present our data in a scoring manner. We did not correlate lactate concentration in fetal blood with neonatal outcomes, as this was not the objective of the study. Actions taken due to CTG findings and FBS results make even short-term neonatal outcome measures such as HIE and UA-pH < 7.00 rare, demanding a larger sample size. Earlier studies have shown good correlations between fetal scalp blood lactate and neonatal outcomes, and the cut-off value for recommendation of intervention has been set well below values predicting low UA-pH and HIE [8, 13]. This is crucial for a diagnostic test as the most important issue must be to have no false-negative tests, i.e., no lactate concentration in normal range and the baby born with metabolic acidosis. As an increased lactate concentration in fetal scalp blood is an early marker in the hypoxic process, the analysis makes birth acidemia largely preventable if proper action is taken [10]. However, intrapartum diagnosis of fetal metabolic acidemia cannot prevent birth acidemia related to chronic fetal hypoxia, where damage might have already occurred before admission to the labor ward, or in obstetric emergencies, such as cord prolapse, placental abruption, or uterine rupture.
Conclusion Isolated reduced variability is not associated with increased rate of fetal acidemia, and this CTG pattern does
not require repeated FBS throughout labor. Severe variable decelerations and late decelerations correlate equally with fetal acidemia. Acknowledgments: We acknowledge the late professor Ingemar Ingemarsson for his valuable input regarding division of CTG patterns.
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