HIGH-RISK PREGNANCY SERIES: AN EXPERT’S VIEW
Problems With Intrapartum Fetal Heart Rate Monitoring Interpretation and Patient Management Roger K. Freeman, MD Fetal heart rate (FHR) monitoring was introduced over 3 decades ago into clinical use and patient management. It continues to be the predominant method for intrapartum fetal surveillance despite questions about its efficacy and outcomes associated with its use. Currently, there appears to be a consensus regarding the reassuring value of a normal reactive pattern without decelerations. Patterns containing absent variability associated with persistent late decelerations, severe variable decelerations, and prolonged decelerations are generally believed to be ominous and may correlate with hypoxia of such severity that fetal central nervous system (CNS) damage may already have occurred. The clinician, however, is faced with FHR patterns between these extremes, and there appears to be a lack of consensus about their management. Furthermore, there is recent evidence that a fetal inflammatory response may lead to CNS damage, and the FHR patterns associated with this condition are not yet understood nor are there any intervention strategies that have been shown to benefit such fetuses. This article is an attempt to illustrate these situations and offer an approach useful to the clinician faced with such FHR patterns. (Obstet Gynecol 2002;100: 813–26. © 2002 by The American College of Obstetricians and Gynecologists.)
Before the introduction of intrapartum electronic fetal heart rate (FHR) monitoring, most fetal deaths that occurred during labor were without warning. Although it was understood that fetal bradycardia detected by auscultation sometimes was associated with “fetal distress,” most interventions that occurred because of fetal bradycardia resulted in the delivery of a fetus that appeared to be well oxygenated. In fact, an analysis of the collaborative project auscultated FHR data by Benson concluded that there was “no reliable indicator of fetal distress in terms of fetal heart rate save in extreme degree.”1 From the Department of Obstetrics and Gynecology, Long Beach Memorial Medical Center, Long Beach, California. We would like to thank the following individuals who, in addition to members of our Editorial Board, will serve as referees for this series: Dwight P. Cruikshank, MD, Ronald S. Gibbs, MD, Gary D. V. Hankins, MD, Philip B. Mead, MD, Kenneth L. Noller, MD, Catherine Y. Spong, MD, and Edward E. Wallach, MD.
Even though there were no reliable data to support a diagnosis of “fetal distress,” it was commonly believed that the major cause of cerebral palsy was asphyxia occurring during the intrapartum period.2– 6 Even in the mid-1970s it was believed that more than half of the cases of mental retardation were due to intrapartum asphyxia and that electronic FHR monitoring could potentially prevent it.7 Early studies of electronic FHR monitoring largely compared its use with historical controls, and none of these studies were randomized. These early studies pointed to the benefit of electronic FHR monitoring relative to auscultated controls. One large analysis of these studies in the aggregate concluded that intrapartum fetal death was significantly less common in patients who were observed with electronic FHR monitoring than in those who had auscultation as it was practiced before electronic FHR monitoring.8 When the randomized controlled trials (RCTs) were undertaken in the 1970s and 1980s the intrapartum fetal death rate did not differ in the auscultated control patients, but the auscultation was done with a one-on-one nurse listening every 15 minutes in the first stage of labor and every 5 minutes in the second stage of labor. Thus, it would appear that continuous electronic FHR monitoring and intensive auscultation are equivalent for the prevention of fetal death and both are superior to the type of auscultation that was done before electronic FHR monitoring. It is probable that intensive monitoring by either electronic or auscultatory means does decrease the intrapartum fetal death rate (a systematic MEDLINE search via PubMed from January 1, 1960 to August 31, 2002 using the search terms “electronic fetal monitoring” and “randomized controlled trial” was performed; no randomized controlled trials of electronic intrapartum fetal monitoring that used no auscultation in the control group were found). There were six RCTs comparing electronic FHR monitoring with intensive auscultation in term patients, and no difference was found with respect to perinatal mortality, Apgar scores, or neonatal intensive care unit admissions.9 –14 Thus, it would appear that electronic FHR monitoring is equivalent to intensive auscultatory monitoring during labor. Because electronic FHR mon-
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Figure 1. Late deceleration with absent variability. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
itoring and intensive auscultatory monitoring both are better than nonintensive auscultatory monitoring in the prevention of intrapartum fetal death, it is interesting
that there has been no reduction in the incidence of cerebral palsy since the introduction and nearly universal use of electronic FHR monitoring. Disappointment in
Figure 2. Severe variable deceleration with absent variability. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
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Figure 3. Prolonged deceleration with absent variability. The fetus died (53759) after 18 minutes of prolonged deceleration. After fetal death occurred, the maternal heart rate was recorded from the fetal scalp electrode. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
the outcomes associated with electronic FHR monitoring may be related to a number of possibilities: 1) A large proportion of asphyxial damage begins before labor and may not benefit from electronic FHR monitoring–prompted interventions occurring during labor. 2) Sudden acute total or near total asphyxia associated with such problems as prolapsed cord, ruptured uterus, ruptured vasa previa, sudden abruption, maternal cardiorespiratory collapse, and shoulder dystocia may not allow sufficient time for intervention before damage is done. 3) A larger proportion of surviving very low birth weight neonates undoubtedly contributes to the current pool of children with cerebral palsy. 4) The recently recognized contribution of infection producing a fetal inflammatory response may be re-
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sponsible for a large percentage of patients who have abnormal electronic FHR monitoring patterns and later develop cerebral palsy. It is unknown if there is a benefit from earlier intervention in such cases. 5) Because the amount of asphyxia required to cause permanent neurological damage is very near the amount that causes fetal death, the number of patients who develop cerebral palsy caused by intrapartum asphyxia is probably quite small. Because of the difficulty in determining if intrapartum asphyxia causes cerebral palsy in a given case, The American College of Obstetricians and Gynecologists (ACOG) issued a technical bulletin in 199215 concluding that, for perinatal asphyxia to be linked to a neurological deficit in the child, all of the following criteria must be present: 1) profound umbilical artery metabolic or mixed acidemia (pH ⬍ 7.00), 2) persistence of an Apgar
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Figure 4. Accelerations with uterine contractions are reassuring. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
score of 0 –3 for longer than 5 minutes, 3) neonatal neurological sequelae (eg, seizures, coma, hypotonia), and 4) multiorgan system dysfunction (eg, cardiovascular, gastrointestinal, hematologic, pulmonary, renal).
In 1995 the Task Force on Cerebral Palsy and Neonatal Asphyxia of the Society of Obstetricians and Gynaecologists of Canada issued a policy statement16 in which they stated that the same criteria mentioned by
Figure 5. Late decelerations with accelerations and good variability. Note that the fetal scalp blood pH in the third panel is 7.35. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
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Figure 6. Mixed variable and late decelerations. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
ACOG must all be present, plus an umbilical artery base deficit of ⱖ16 mmol/L. They stated that if all of these criteria are not present we cannot conclude that hypoxic acidemia exists or has the potential to cause neurological deficits during the intrapartum period. In 1999 Alastair MacLennan published a consensus statement of the Perinatal Society of Australia and New Zealand endorsed by some 21 obstetric and pediatric societies from around the world and prepared by some 49 people from seven countries.17 The following were the document’s essential criteria for defining an acute intrapartum hypoxic event sufficient to cause permanent neurological impairment: 1) Evidence of metabolic acidosis in intrapartum fetal umbilical arterial cord or very early neonatal blood samples (pH ⬍ 7.00 and base deficit ⱖ 12 mmol/L) 2) Early onset of severe or moderate neonatal encephalopathy in infants of ⱖ34 weeks’ gestation 3) Cerebral palsy of the spastic quadriparetic or dyskinetic type Criteria that together suggest an intrapartum timing but by themselves are nonspecific 4) A sentinel (signal) hypoxic event occurring immediately before or during labor
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5) A sudden, rapid, and sustained deterioration of the FHR pattern usually after the hypoxic sentinel event where the pattern was previously normal 6) Apgar scores of 0 – 6 for longer than 5 minutes 7) Early evidence of multisystem involvement 8) Early imaging evidence of acute cerebral abnormality Unfortunately, debates over causation of neurological damage caused by intrapartum asphyxia usually take place in the courtroom. Nevertheless, it remains clear that about 10% of patients who later develop cerebral palsy have evidence of isolated intrapartum hypoxia as a cause. It is also clear that in some cases intervention may prevent or decrease the severity of cerebral palsy. Animal studies show that patterns of late deceleration can be produced with induced fetal hypoxia. Early work by Kubli and others18 showed that there is a rough correlation between metabolic acidosis and abnormal FHR patterns. Apgar scores have a poor correlation to abnormal FHR patterns. In fact, the majority of fetuses with nonreassuring FHR patterns have Apgar scores of 7 or greater at 5 minutes.19 Nelson20 has shown that FHR patterns are poor predictors of cerebral palsy, but patterns of late deceleration with decreased variability are seen more commonly in fetuses destined to develop cerebral palsy. When FHR monitoring was first introduced, the fol-
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Figure 7. Flat fetal heart rate with no decelerations. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
lowing patterns were considered sufficient to require expeditious delivery: 1) persistent uncorrectable late deceleration, 2) persistent uncorrectable severe variable deceleration, and 3) uncorrectable prolonged deceleration. Since then, the significance of FHR variability has become more important, and there are some who say that as long as variability is present, there is no need to intervene. There are others who say that if one waits until variability is lost, it may be too late. Numerous studies have been done to determine the reproducibility of FHR pattern interpretation between experienced physicians and even in the same individual at different times. The findings in these studies were disappointing in that there was poor agreement between individuals and even some inconsistency when the same
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individual was asked to repeat his or her readings at another time. It was because of the lack of agreement about pattern interpretation as well as the high number of false-positive tracings that the National Institute of Child Health and Human Development decided to convene a conference on this subject. In 1997 the National Institute of Child Health and Human Development Research Planning Workshop on Fetal Monitoring21 concluded that the following patterns are consistent with hypoxia that is predictive of current or impending fetal asphyxia so severe that the fetus is at risk for neurological and other fetal damage or death: 1) Late decelerations with absent variability (Figure 1)
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Figure 8. This patient presented with no prenatal care and was noted to have a fetal heart rate of 60. Because it could not be determined if this was a prolonged deceleration, the fetus was delivered by cesarean delivery, resulting in a neonate with Apgar scores of 8 at 1 and 5 minutes. The neonatal electrocardiogram revealed a complete heart block. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
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Figure 9. Fetal tachycardia with decreased variability. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
2) Variable decelerations with absent variability (Figure 2) 3) Sustained bradycardia with absent variability (Figure 3)
●
They also concluded that patterns with all of the following characteristics confer a high probability of a normally oxygenated fetus (Figure 4).
Although there is no agreement about the significance of the above patterns, some of them are present in fetuses that subsequently develop neonatal encephalopathy and, later, cerebral palsy. At the present time, only hypoxia is felt to be a cause of neurological injury that may be alleviated by expeditious delivery. For this reason, a strategy that utilizes other means of fetal evaluation seems appropriate. Originally, fetal scalp blood sampling for pH analysis was used to assess fetuses with abnormal FHR patterns. When Clark et al22 pointed out that the presence of accelerations either spontaneous or evoked can be considered evidence that the fetal pH is above 7.20, fetal scalp pH sampling fell into disfavor. More recently, fetal pulse oxymetry has been introduced for use with these problematic FHR patterns, but its acceptance is still being evaluated.23,24 Additionally, some of the above patterns may reflect fetal central nervous system dysfunction with or without hypoxia and acidosis, and in such situations FHR acceleration may not be present or evoked, so that either fetal scalp blood pH sampling or fetal pulse oxymetry may be helpful (Figure 14). Recently, the presence of infection has been found to
1) 2) 3) 4)
Normal baseline rate Normal (moderate) FHR variability Presence of FHR accelerations Absence of FHR decelerations
There are FHR patterns that meet neither of the above ominous or reassuring criteria, and a consensus has not been developed for management of patients whose patterns are in between. The next section attempts to illustrate some of these problematic tracings. ● ● ● ● ● ●
Late decelerations with good variability and accelerations (Figure 5) Variable decelerations with slow return or a late component (Figure 6) Absent variability with no decelerations associated with contractions (Figure 7) Fetal heart block (Figure 8) Fetal tachycardia without decelerations (Figure 9) Sinusoidal patterns (Figure 10)
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Blunted patterns (Figure 11) Checkmark pattern (Figure 12) Twins, one flat and one reactive (Figure 13)
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Figure 10. Sinusoidal pattern in a fetus undergoing antepartum testing for maternal hypertension. The neonate had a hematocrit of 9%. Of the maternal red blood cells, 3.5% were fetal, indicating a fetal maternal hemorrhage. The neonate had a difficult course but survived and developed normally. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
be an important finding in fetuses that are destined to develop cerebral palsy. The fetal inflammatory response associated with maternal fever during labor, choriamnionitis, and funisitis has been implicated as a cause of later cerebral palsy.25–27 It is believed that inflammatory cytokines can cause cerebral ischemia resulting in damage to the paraventricular area of premature fetal brains.28 –32 These lesions appear as periventricular leukomalacia and intraventricular hemorrhage. The relation between chorioamnionitis and cerebral palsy in term fetuses has been demonstrated by Grether and Nelson.33,34 Cytokines have also been implicated in term fetuses.35 As our knowledge of infectious causes of cerebral palsy increases, it may account for some of the large percentage of cerebral palsy with unknown cause and strategies for intervention may become evident. At this time we do not know what FHR patterns are associated
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with fetal infection. In fact, it is possible that the cytokines elaborated in such cases could cause ischemia of the umbilical or uterine vessels and result in variable or late deceleration, and the fetus may become hypoxic and acidotic. The following are interesting FHR patterns that were associated with later cerebral palsy in fetuses with infection (Figures 15 and 16). In conclusion, there are many FHR patterns that lie between the completely reassuring patterns and those considered ominous by the National Institute of Child Health and Human Development task force, which cannot be ignored and require another assessment by methods including fetal scalp stimulation, fetal scalp blood pH, or fetal pulse oximetry. In addition, new knowledge about infection and inflammatory cytokines may point to possible explanations for cerebral palsy that were
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Figure 11. Blunted variable decelerations with absent variability. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
Figure 12. Checkmark pattern in a fetus whose mother had undergone a cardiorespiratory arrest and was subsequently resuscitated. The newborn was born with a normal pH but immediately began having seizures, and the child now has central nervous system damage. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
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Figure 13. Tracing of twins revealing a flat pattern in one twin (A) and a normal reactive pattern in the co-twin (B). Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
Figure 14. A flat pattern with an unstable baseline but no periodic late or variable decelerations. Note the pH of 6.91 in the middle of the third panel. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
Figure 15. Fetal tachycardia associated with maternal fever. The fetal scalp pH was 7.23. This fetus had a difficult neonatal course, and the child now has central nervous system damage. There was evidence of chorioamnionitis and funisitis. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
Figure 16. This patient entered labor with a temperature of 38C. The initial fetal heart rate pattern was tachycardia, but subsequently a blunted pattern developed. The cord pH was 6.72 and the amniotic fluid culture indicated Staphylococcus aureus. The child developed spastic quadriparesis. Freeman. FHR Monitoring Interpretation. Obstet Gynecol 2002.
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previously unappreciated and FHR patterns that are atypical. Certainly, at this time, there are no strategies that have been shown to alter the outcome in cases of infection and the fetal inflammatory syndrome. REFERENCES 1. Benson RC, Schubeck F, Deutschberger J, Weiss W, Berendes H. Fetal heart rate as a predictor of fetal distress: A report from the collaborative project. Obstet Gynecol 1968;32:259 – 66. 2. Little WJ. On the influence of abnormal parturition, difficult labours, premature birth and asphyxia neonatorum, on the mental and physical condition of the child, especially in relation to deformities. Trans Obstet Soc Lond 1862;3:293. 3. Lilienfeld AM, Pasamanick B. The association of maternal and fetal factors with the development of cerebral palsy and epilepsy. Am J Obstet Gynecol 1955;70:93. 4. Eastman NJ, DeLeon M. The etiology of cerebral palsy. Am J Obstet Gynecol 1955;69:950. 5. Eastman NJ, Kohl SG, Maisel JE, Kavaler F. The obstetrical background of 753 cases of cerebral palsy. Obstet Gynecol Surv 1962;17:459 –500. 6. Steer CW, Bonney W. Obstetric factors in cerebral palsy. Am J Obstet Gynecol 1962;83:526. 7. Quilligan EJ, Paul RH. Fetal monitoring: Is it worth it? Obstet Gynecol 1975;45:96 –100. 8. Antenatal diagnosis. Report of a consensus development conference. NIH publication no. 79-1973. Bethesda, MD: National Institutes of Health, 1979. 9. Haverkamp AD, Thompson HE, McFee JG, Cetrulo C. The evaluation of continuous fetal heart rate monitoring in high risk pregnancy. Am J Obstet Gynecol 1976;125: 310 –20. 10. Haverkamp AD, Orleans M, Langendoerfer S, McFee J, Murphy J, Thompson HE. A controlled trial of the differential effects of intrapartum fetal monitoring. Am J Obstet Gynecol 1979;134:399 – 412. 11. Renou P, Chang A, Anderson I, Wood C. Controlled trial of fetal intensive care. Am J Obstet Gynecol 1976;126: 470 – 6. 12. Kelso IM, Parsons RJ, Lawrence GE, Arora SS, Edmonds DK, Cooke ID. An assessment of continuous fetal heart rate monitoring in labor: A randomized trial. Am J Obstet Gynecol 1978;131:526 –32. 13. Wood C, Renou P, Oates J, Farrell E, Beischer N, Anderson I. A controlled trial of fetal heart rate monitoring in a low-risk population. Am J Obstet Gynecol 1981;141: 527–34. 14. McDonald D, Grant A, Sheridan-Pereira M, Boylan P, Chalmers I. The Dublin randomized control trial of intrapartum fetal heart rate monitoring. Am J Obstet Gynecol 1985;152:524 –39.
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15. American College of Obstetricians and Gynecologists. Fetal and neonatal neurologic injury. ACOG technical bulletin no. 163. Washington, DC: American College of Obstetricians and Gynecologists, 1992. 16. Policy statement of the Task Force on Cerebral Palsy and Neonatal Asphyxia of the Society of Obstetricians and Gynecologists of Canada (part I). J Soc Obstet Gynecol Can 1996;1267–79. 17. MacLennan A. A template for defining a causal relationship between acute intrapartum events and cerebral palsy—an international consensus statement. BMJ 1999;319: 1054 –9. 18. Kubli F, Hon E, Khazin A, Takemura H. Observations on fetal heart rate and pH in the human fetus during labor. Am J Obstet Gynecol 1969;104:1190 –206. 19. Schifrin B, Dame L. Fetal heart rate prediction of Apgar score. JAMA 1972;219:1322–5. 20. Nelson KB, Dambrosia JM, Ting TY, Grether JK. Uncertain value of fetal heart rate monitoring in predicting cerebral palsy. N Engl J Med 1996;334:613– 8. 21. National Institute of Child Health and Human Development Research Planning Workshop. Electronic fetal heart rate monitoring: Research guidelines for interpretation. Am J Obstet Gynecol 1997;177:1385–90. 22. Clark SL, Gimovsky ML, Miller FC. The scalp stimulation test: A clinical alternative to fetal scalp blood sampling. Am J Obstet Gynecol 1984;148:274 –7. 23. Garite TJ, Dildy GA, McNamara H, Nageotte MP, Bohem FH, Dellinger EH. A multicenter controlled trial of fetal pulse oximetry in the intrapartum management of nonreassuring fetal heart rate patterns. Am J Obstet Gynecol 2000;183:1049 –58. 24. American College of Obstetricians and Gynecologists. Fetal pulse oximetry. ACOG committee opinion no. 258. Obstet Gynecol 2001;98:523– 4. 25. Dammann O, Leviton A. Role of the fetus in perinatal infection and neonatal brain damage. Curr Opin Pediatr 2000;12:99 –104. 26. Lieberman Richardson DK, Lang J, Frigoletto FD, Heffner LJ, Cohen A. Intrapartum maternal fever and neonatal outcome. Pediatrics 2000;105:8 –13. 27. Impey L, Greenwood C, MacQuillan K, Reynolds M, Sheil O. Fever in labour and neonatal encephalopathy: A prospective cohort study. Br J Obstet Gynecol 2001;108:594 –7. 28. Yoon BH, Jun JK, Romero R, Park KH, Gomez R, Choi JH. Amniotic fluid inflammatory cytokines (interlukin 6, interleukin 1B, and tumor necrosis factor a), neonatal white matter lesions, and cerebral palsy. Am J Obstet Gynecol 1997;177:19 –26. 29. Yoon BH, Romero R, Park JS, Kim CJ, Kim SH, Choi JH, et al. Fetal exposure to an intra-amniotic inflammation and the development of cerebral palsy at the age of three years. Am J Obstet Gynecol 2000;182:675– 81. 30. Naccasha N, Hinson R, Montag A, Ismail M, Bentz L, Mittendorf R. Association between funisitis and elevated
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interleukin-6 in cord blood. Obstet Gynecol 2001;97: 220 – 4. 31. Dammann O, Leviton A. Maternal intrauterine infection, cytokines, and brain damage in the preterm newborn. Pediatr Res 1997;42:1– 8.
34. Eschenbach DA. Amniotic fluid infection and cerebral palsy [editorial]. JAMA 1997;278:247– 8. 35. Nelson KB, Dambrosia JM, Grether JK, Phillips TM. Neonatal cytokines and coagulation factors in children with cerebral palsy. Ann Neurol 1998;44:666 –75.
32. Steinborn A, Niederhut A, Solbach C, Hildenbrand R, Sohn C, Kaufmann M. Cytokine release from placental endothelial cells, a process associated with pre-term labour in the absence of intrauterine infection. Cytokine 1999;11: 66 –73.
Address reprint requests to: Roger K. Freeman, MD, Long Beach Memorial Medical Center, Department of Obstetrics and Gynecology, 2801 Atlantic Avenue, Long Beach, CA 90801; E-mail:
[email protected].
33. Grether JK, Nelson LB. Maternal infection and cerebral palsy in infants of normal birth weight. JAMA 1997;278: 207–11.
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Received March 25, 2002. Received in revised form April 18, 2002. Accepted May 13, 2002.
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