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INTRAPARTUM FETAL SURVEILLANCE
ANTEPARTUM AND INTRAPARTUM FETAL ASSESSMENT
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INTRAPARTUM FETAL SURVEILLANCE Is It Worthwhile? James A. Low, MD
Screening in an attempt to prevent disease is attractive in comparison with the traditional medical model of reacting to disease. Prevention avoids morbidity and mortality and offers a way of reducing expensive medical care. Although for many years screening has been considered to be harmless, a growing body of evidence suggests that screening can harm individuals, particularly via the adverse effects of false-positive and false-negative results.59The skepticism regarding the benefits of screening has been highlighted by the first annual report of the National Screening Committee in the United Kingdom.4l That report concluded that only 4 of 100 screening programs in clinical practice met the criteria for quality or evidence of effectiveness. Two questions must be addressed regarding the current surveillance of the fetus during labor: (1)the clinical problem of whether the significance of intraparturn fetal asphyxia justifies intervention to provide fetal surveillance, and (2) the fetal surveillance problem of whether the benefits outweigh the harm. CLINICAL PROBLEM
Understanding of the association between fetal asphyxia and brain damage is based on research in the fetal monkey and lamb. Studies of From the Departments of Obstetrics and Gynaecology and Paediatrics, Queen’s University, Kingston, Ontario, Canada
OBSTETRICS AND GYNECOLOGY CLINICS OF NORTH AMERICA
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global asphyxia9,3z, 35, 53 and cerebral ischemia3" have confirmed that exposure of more than 10 minutes is associated with brain damage. Studies of partial asphyxias,13, 39, have demonstrated that sustained partial asphyxia of 1 to 3 hours may or may not be associated with brain damage. The key to the occurrence of brain damage is severe fetal metabolic acidosis and cardiovascular decompensation with systemic hypotension. Clinical studies require a definition and diagnostic criteria of potentially significant fetal asphyxia. A task force set up by the World Federation of Neurology Group defined asphyxia as a condition of impaired gas exchange leading, if it persists, to progressive hypoxemia and hypercapnia.4 According to this definition, asphyxia may occur in a transient fashion, which although of physiologic interest, has no pathologic significance. Pathology owing to asphyxia is caused by progressive hypoxemia leading to tissue oxygen debt with accumulation of fixed acids and a metabolic acidosis; therefore, the following addition has been proposed for the definition of potentially significant intraparturn fetal asphyxia3? Fetal asphyxia is a condition of impaired blood gas exchange leading, if it persists, to progressive hypoxemia and hypercapnia with a metabolic acidosis.
This definition serves as a reminder that the definitive diagnosis of asphyxia requires a blood gas and acid-base assessment. The important question for fetaI asphyxia is the threshoId of metabolic acidosis beyond which fetal morbidity and mortality may occur. A series of clinical studiesZ7, z8, 31 have demonstrated that the threshold of metabolic acidosis beyond which moderate and severe newborn complications and particularly newborn encephalopathy begin to occur is an umbilical artery base deficit greater than 12 mmol/L. The frequency of moderate and severe newborn complications in relation to the degree of metabolic acidosis is summarized in Table 1. There is a threshold of asphyxia1 exposure expressed by umbilical artery base deficit beyond which some newborns may and some newborns may not have evidence of brain dysfunction or other organ system complications. Brain dysfunction may be reversible and the clinical manifestations transient. In other cases, particularly those with severe newborn encephalopathy, brain damage may occur and account for subsequent motor
Table 1. FREQUENCY OF MODERATE OR SEVERE NEWBORN COMPLICATIONS IN RELATION TO DEGREE OF METABOLIC ACIDOSIS AT DELIVERY ~~
~
~~
Metabolic Acidosis Umbilical Artery Base Deficit
~~
Newborn Complications Moderate or Severe
12-16 -ol/L
10%
>16 mmol/L
40%
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and cognitive deficits. The occurrence of motor and cognitive deficits after biochemically confirmed intrapartum fetal asphyxia has been exam26 Many children demonstrated ined in term and preterm ne~borns.2~. normal motor and cognitive development at 1 year of age. Nevertheless, in both studies, there was a significant increase in the occurrence of motor and cognitive deficits or brain damage in early neonatal deaths after fetal asphyxia in the term and preterm newborns. These clinical studies emphasize that despite the occurrence of newborn and long-term morbidity after intrapartum fetal asphyxia, a large number of infants do not exhibit evidence of newborn brain dysfunction or subsequent clinical manifestations of brain damage. Current understanding of the variable outcome after fetal asphyxia is based on the concept of fetal cardiovascular compensation developed in research studies in the fetal lamb. The effect of fetal asphyxia owing to maternal hyp~xemia,~,56, 57 reduced uteroplacental blood flow? 21, 30, 54 and cord o c c l ~ s i o non ~ , ~fetal ~ cardiovascular function has been examined. There has been a remarkable consistency of the fetal cardiovascular response in these different models. The initial response to an asphyxia1 exposure is an increase of arterial pressure owing to increased systemic vascular resistance mediated by the autonomic nervous system.22There is a redistribution of cardiac output, with decreased blood flow to the lungs, kidney, gastrointestinal system, and body and a centralization of circulation with increased blood flow to the brain, heart, and adrenals. This cardiovascular response is important to the integrity of the central nervous system. Cerebral oxygen requirements are reduced with an increase of highvoltage electrocortical Cerebral oxygen metabolism is maintained because of a combination of increased cerebral blood flow and oxygen extraction. A classification of the severity of an asphyxial exposure is required to predict the long-term outcome in the child. The significance of fetal asphyxia depends on several factors, including the degree, duration, and nature (continuous or intermittent) of the asphyxial exposure and the quality of the fetal cardiovascular response. In the clinical setting, a measure of the degree of metabolic acidosis confirms that an asphyxial exposure has occurred; however, information regarding the duration and nature of the exposure and the fetal cardiovascular response is generally not available. A classification of the severity of intrapartum fetal asphyxia has been proposed by determining the short-term outcome as expressed by newborn encephalopathy and other newborn organ system complications (Table 2).3O This classification is based on the evidence that early-onset newborn encephalopathy is the best single predictor of longterm outcome. In a review of five studies of term newborns, Pelowski and FineP reported a good outcome for newborns with minor newborn encephalopathy, whereas the risk of death or severe disability was 5.6% and 20% for newborns with moderate encephalopathy and 60% and 72% for newborns with severe encephalopathy, respectively. Cardiovascular, respiratory, and particularly renal complications provide a further indi-
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Table 2. CLASSIFICATIONOF INTRAPARTUMFETAL ASPHYXIA
Degree of Asphyxia ~
Mild Moderate Severe
Metabolic Acidosis at Delivery*
+ + +
Cardiovascular, Respiratory, and Renal Complications
Encephalopathy Minor ~~
*
Moderate
Severe
Minor
Moderate to Severe
f
+
f
+
+
+
= present; & = present or absent. ‘Umbilical artery base defiats 212 mmol/L. From Low JA: Intraparturn fetal asphyxia: Definition, diagnosis and classification. Am J Obstet Gynecol 176:957-959, 1997; with permission.
cation of the severity of the asphyxial exposure in both term and preterm newborns. Evidence is now available to define the magnitude of the clinical problem of intrapartum fetal asphyxia. Routine blood gas and acid-base assessment of umbilical artery blood at delivery have demonstrated an umbilical artery base deficit of greater than 12 mmol/L in 2% and of greater than 16 mmol/L in 0.5%of the total population. Table 3 summarizes the clinical problem based on the current understanding of the occurrence of moderate and severe newborn encephalopathy in these categories of metabolic acidosis and of subsequent death or severe disability in relation to the severity of newborn encephalopathy. Moderate or severe asphyxia occurs in 3 to 4 per 1000 births, of which approximately 1 per 1000 has evidence of brain damage. INTRAPARTUM FETAL SURVEILLANCE
The goal of intrapartum fetal surveillance is to reduce the incidence of fetal asphyxial exposure and to prevent moderate and severe asphyxia. Because intrapartum fetal asphyxia is usually partial and often Table 3. MAGNITUDE OF THE CLINICAL PROBLEM OF INTRAPARTUM FETAL ASPHYXIA ~
~
~~
Outcome per 1000 Births Umbilical Artery Base Deficit Event
Asphyxia1 exposure Mild Moderate/severe Asphyxia with brain damage
12-16 mmoUL
>16 mmoUL
15.0 13.5
5.0 3.0 2.0
\
1
J
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intermittent, fetal compensation may be satisfactory for some time (hours). This interval provides a window of opportunity during which the occurrence of an asphyxial exposure can be confirmed, and, when appropriate, intervention can be initiated before the threshold of decompensation has been reached. A clinical paradigm for the prediction and diagnosis of intrapartum fetal asphyxia emerged in the 1960s as a result of three developments: clinical risk scoring, electronic fetal heart rate monitoring (EFM), and microelectrodes permitting fetal blood gas and acid-base assessment. It was proposed that clinical risk scoring would identify pregnancies at risk for intraparturn fetal asphyxia, that continuous EFM of risk pregnancies would identify the fetus experiencing an asphyxial exposure, and that blood gas and acid-base assessment of fetal blood would confirm the fetal asphyxia with a developing metabolic acidosis. Clinical Risk Scoring
Two studies have highlighted the limitations of clinical risk 29 Fetal exposure to asphyxia occurs in pregnancies with no clinical risk factors. This observation was made in 23% of pregnancies with a potentially significant metabolic acidosis at delivery and in 40% of perinatal deaths with postmortem evidence of brain damage owing to antepartum or intrapartum fetal asphyxia. In cases in which clinical risk factors were present, risk was determined by a wide range of complications, with no single risk factor demonstrating a strong association with intrapartum fetal asphyxia. The positive predictive value for antepartum and intrapartum risk factors was 3%, with a low predictive value for each individual risk factor. Clinical risk scoring has a major problem of false-positive prediction of intrapartum fetal asphyxia. Clinical risk scoring is a valuable method of assessment of the obstetric patient and her pregnancy; however, clinical risk scoring is of limited predictive value for intrapartum fetal asphyxia. There are no low-risk pregnancies for intraparturn fetal asphyxia. Because of the major problem of false-positive findings, at-risk pregnancies require supplementary tests to justify intervention for suspected fetal asphyxia. Electronic Fetal Heart Rate Monitoring
Fetal heart rate observations began in the nineteenth century, whereas EFM was developed in the twentieth century.l5,6o Despite this long history, the value of intermittent fetal heart rate auscultation and continuous EFM in the prediction of intrapartum fetal asphyxia has yet to be established. The evidence to date indicates that EFM has been associated with
a reduction in the number of intraparturn fetal deaths5' 65; however, intrapartum deaths continue to occur. A national study of stillbirths in England and Wales between 1993 and 1995 reported that 10% of stillbirths occurred in the intraparturn period, most of which were attributed to asphyxia.' Limited evidence suggests an association between abnormal fetal heart rate patterns and neurologic abnormality in surviving ~hildren.'~, 46 In a retrospective study of children with cerebral palsy, Rosen and D i c k i n s ~ nfailed ~ ~ to find a consistent fetal heart rate pattern that would predict brain injury. It was concluded that these findings should not be surprising because most brain damage occurs outside the intraparturn period. Well-designed randomized clinical trials have been proposed to minimize selection bias and to determine the true risks and benefits of a medical intervention. No randomized clinical trials have compared no fetal heart rate surveillance with intermittent fetal heart rate auscultation. The value of EFM is increasingly questioned because of recently reported randomized trials of this test?" EFM has failed to provide consistent evidence of decreased fetal or newborn morbidity or mortality. Two confounding factors may be the numbers in the study population and the modified clinical management in study protocols. Nevertheless, the trials to date have made an important contribution, demonstrating that EFM has been associated with unnecessary intervention, with an increased incidence of cesarean delivery for fetal distress and dystocia, operative delivery, and general anesthesia." These findings emphasize the need for a better understanding of the predictive limitations of EFM. Laboratory evidence indicates that fetal heart rate assessment should be of value in the prediction of fetal asphyxia. Studies in the fetal lamb have demonstrated a relationship between late decelerations and fetal hypoxemia and metabolic acidosis. Late decelerations have been shown to occur when fetal oxygen tension decreases below a critical level. The interval between the onset of the contraction and the onset of the deceleration reflects the time necessary for the fetal oxygen tension to fall below this threshold.20,37, 38 Late decelerations in relation to fetal hypoxemia in a previously normoxic fetus are the result of chemoreceptor-initiated reflex bradycardia, which can be blocked by atropine, whereas in the previously hypoxic fetus, the bradycardia may be the result of a direct effect on the myocardium.3'jr49 It has been difficult to provide evidence that the benefits of EFM outweigh the harm as a test of fetal assessment. Three factors may account for these equivocal results: Asphyxia may occur before the onset of labor. Methodologic issues may exist in regards to the assessment protocol and fetal heart rate interpretation. Limitations may apply to the predictive value of fetal heart rate patterns.
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Anteparturn Fetal Asphyxia
Fetal asphyxia may occur in the antepartum period. The significance of antepartum fetal complications including asphyxia was implied in the data from the National Collaborative Perinatal Project, which determined that when all principal risk factors present by the time that labor began were considered, 5% of the population at highest risk contributed to 34% of the cases of cerebral pal~y.4~ The occurrence of antepartum brain damage has been demonstrated in postmortem studies. Studies of stillbirths and early neonatal deaths indicate that a sublethal asphyxial exposure in the preterm and term fetus prior to the onset of labor can cause brain damage with characteristic neuropathologic findings.5,10,12,17,24 Recent antepartum cordocentesis studies have confirmed the occurrence of antepartum fetal asphyxial exposure. Some fetuses, particularly those believed to be growth-retarded, have demonstrated hypoxemia, hypercapnia, and metabolic acidosis prior to the onset of labor.” a5, Nevertheless, there is no information on the prevalence of biochemically confirmed fetal asphyxia in the antepartum period. In the absence of a precise diagnosis, the contribution of antepartum fetal asphyxia to brain damage and neurodevelopmental disability has not been established. This limitation may complicate intrapartum fetal assessment because the assessment during labor may reflect events occurring prior to the onset of labor. Methodologic Issues
Numerous factors may affect the appropriate use of EFM. These include the duration of the assessment, the quality of fetal heart rate data, the classification and interpretation of fetal heart rate variables, and the interpretation of the fetal heart rate record. Ideally, fetal intrapartum surveillance should begin with onset of labor. With the exception of the induction of labor, this timing is rarely achieved. Thus, intrapartum fetal asphyxial exposure may occur before fetal assessment is initiated. When fetal surveillance begins, the duration of the record must be sufficient to permit interpretation of the pattern of fetal heart rate behavior. The quality of the fetal heart rate data must be adequate for interpretation. In 1958, Hon15 reported that electronic techniques provided a more accurate indication of fetal heart rate than was possible with intermittent auscultation. This is true in the classification of baseline fetal heart rate variability and decelerations. The quality of the recording must also be adequate for interpretation. Ultrasound fetal heart rate signal and the tocodynometer have provided an attractive noninvasive option; however, in some cases, the fetal heart rate signal and particularly the uterine contraction waveform may not be satisfactory, in which case a scalp electrode and intrauterine catheter are required.
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Differences of classification criteria remain, particularly for decelerations. In the classification of late decelerations, some clinicians have given first priority to the timing of the nadir of the deceleration, whereas others have emphasized the waveform. In interpretation of the waveform, both the onset to the nadir16 and the residual component of the waveform have been examined.62Efforts to quantify decelerations are continuing."63 Until a consensus is developed, as recently recommended, interpretation criteria should be clearly defined and consistently used.40 Although progress has been made in regards to computer-based interpretation of fetal heart rate records, with few exceptions, clinical records are read visually. The limited interobserver reliability for visual A interpretation of fetal heart rate patterns has been well-d0cumented.4~ recent study at the author's center demonstrated the following good-tofair interobserver Kappa values: baseline fetal heart rate, 0.70; baseline fetal heart rate variability, 0.55; fetal heart rate accelerations, 0.56; variable decelerations, 0.46; and late or prolonged decelerations, 0.57. This limited interobserver reliability of individual fetal heart rate variables can be offset by scoring fetal heart rate patterns. In 20 fetal heart rate records, the classification of fetal heart rate patterns in 1 hour of recording was similar between two observers." The interpretation of fetal heart rate patterns based on variables that have an association with potentially significant metabolic acidosis requires an examination of the fetal heart rate record over time. The record should be scored in 10-minute epochs (cycles). Determination of the pattern requires careful scoring of a number of cycles, which, in most cases, can be achieved with six cycles representing 1 hour of the fetal heart rate record. Predictive Fetal Heart Rate Variables
The fetal heart rate variables associated with intrapartum fetal asphyxia with a potentially significant metabolic acidosis were determined in a matched case-control study performed by the author and his colThe study population included 71 fetuses in the asphyxia group (umbilical artery base deficit >16 mmol/L) and 71 in the control group (umbilical artery base deficit <8 mmol/L). The severity of the asphyxia1 exposure in the asphyxia group was classified as mild (n = 41), moderate (n = 17), or severe (n = 13). Each fetal heart rate record was scored in 10-minute cycles over the last 4 hours of labor. The baseline fetal heart rate variables scored included baseline fetal heart rate and baseline fetal heart rate variability. The periodic fetal heart rate variables scored included accelerations and variable, early, late, and prolonged decelerations. Three fetal heart rate variables (baseline fetal heart rate, variable, and early decelerations) did not discriminate between the asphyxia and
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control groups. One fetal heart rate variable (spontaneous accelerations) had an association with the control group. Three fetal heart rate variables (baseline fetal heart rate variability, late decelerations, and prolonged decelerations)had a significant association with the asphyxia group during the last hour of the fetal heart rate record; however, no single fetal heart rate variable occurred in all asphyxia cases, and each fetal heart rate variable occurred in the absence of fetal asphyxia. Each predictive fetal heart rate variable may occur in one cycle or two or more cycles and may occur independently or in combination with another fetal heart rate variable; therefore, fetal heart rate patterns based on the findings in six 10-minute cycles of recording are required to determine the predictive value of repetitive combined fetal heart rate variables for asphyxia. The fetal heart rate patterns examined in the author’s study were absent baseline variability, usually with repetitive cycles (two or more) of late or prolonged decelerations; repetitive cycles (two or more) of minimal baseline fetal heart rate variability and late or prolonged decelerations; repetitive cycles (two or more) of either minimal baseline fetal heart rate variability or late or prolonged decelerations; and one cycle of either minimal baseline fetal heart rate variability or late or prolonged decelerations. Absent baseline fetal heart rate variability with repetitive late or prolonged decelerations occurred principally in the asphyxia group. In the remaining cases, the association with asphyxia decreased with decreasing frequency of cycles of minimal baseline variability and late or prolonged decelerations or both. The sensitivity of fetal heart rate patterns is outlined in Figure 1. Fetal heart rate patterns with absent baseline variability identified 17% of the asphyxia group and 36% of the moderate and severe asphyxia group. The sensitivity increased to 93% with the addition of less specific patterns. The predictive value of fetal heart rate patterns is outlined in Figure 2. Fetal heart rate patterns with absent baseline variability are most specific, with occasional false-positive findings. The remaining patterns have a low positive predictive value. The prediction of fetal asphyxia by fetal heart rate patterns is possible but difficult. The prediction of moderate and severe asphyxia, that is, after fetal cardiovascular decompensation has occurred, is not consistent with the goal of intrapartum fetal monitoring, thus prediction cannot wait for absent baseline fetal heart rate variability. The possibility of asphyxia must be considered when there is a 1-hour window with two or more cycles of minimal baseline variabiIity and late or prolonged decelerations or both. The potential for unnecessary intervention is great using these criteria. Because intrapartum fetal asphyxia is an infrequent event and because fetal heart rate patterns are not specific, there are a large number of false-positive fetal heart rate patterns.
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100
4-
c
a,
60-
e
a, R
40-
20
-
0-
FHR Pattern FHR Variability Absent (cycles)
I
2
+
3
+
4
-
>I 72
52
I
and
and
or
or
52
52
52
I
Minimal (cycles)
Late & prolonged
+
Decelerations
(cycles)
Figure 1. Fetal heart rate patterns-sensitivity. A sensitivity for prediction of fetal asphyxia of 93% can be achieved if all fetal heart rate patterns with minimal baseline variability and late or prolonged decelerations are included. Open bars = mild and moderatelsevere asphyxia; and solid bars = moderatelsevereasphyxia.
Supplementary Tests
If EMF is to be used as a screening test for intrapartum fetal asphyxia, predictive fetal heart rate patterns require supplementary tests to confirm the diagnosis of fetal asphyxia and to identify false-positive tests to avoid unnecessary intervention. A number of supplementary tests are currently being assessed, including fetal vibroacoustic stimulation, the ST segment and PR interval of the fetal electrocardiogram, fetal pulse oximetry fetal pH electrode, and near-infrared spectroscopy. Although potential benefits have been reported, particularly in the identification of false-positive fetal heart rate patterns, the clinical value of these tests remains to be determined. A fetal blood gas and acid-base assessment with evidence of a metabolic acidosis is the gold standard for the diagnosis of fetal asphyxia. The occurrence or exclusion of intrapartum fetal asphyxia can be confirmed by a blood gas and acid-base assessment of umbilical vein and artery blood at delivery without compromising either the gravida or fetus. If moderate and severe intrapartum fetal asphyxia are to be prevented, the occurrence of asphyxia1 exposure with a developing metabolic acidosis must be confirmed before delivery. A scalp sample of fetal
LNTRAI'ARTUM FETAL SURVEILLANCE
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100
80 c
c
al
eal
a
-
60,40-
20
I
0
FHR Pattern
I
+
2
+
3
+
4
FHR Variability Absent (cycles) Minimal (cycles) Late & prolonged Decelerations
5I
and 32
52
52
and
or
52
or I
Figure 2. Fetal heart rate patterns-predictivevalue. False-positiveprediction is a frequent occurrence with fetal heart rate patterns including minimal baseline variability and late or prolonged decelerations. Open bars = true-positive; solid bars = false-positive.
blood for a blood gas and acid-base assessment is currently the only test that can confirm this diagnosis or identify false-positive predictive tests. SUMMARY
Potentially sigruficant intrapartum fetal asphyxia occurs in approximately 20 per 1000 births. Moderate and severe fetal asphyxia exposure with newborn morbidity occurs in 3 to 4 per 1000 births, with brain damage and subsequent disability in at least 1per 1000 births. Although the prevalence of moderate and severe asphyxia is modest, prevention is important because of the serious implications of this complication to the child, family, and society. Because of the limited predictive value of clinical risk factors, the interpretation of patterns in a fetal heart rate record has become the primary screening test for intrapartum fetal asphyxia. Despite extensive clinical experience and numerous clinical trials, the benefits of EFM as a screening test have not been established, and harm may occur owing to unnecessary intervention. This observation raises serious ethical issues. When an intervention is initiated by the clinician rather than the patient, the clinician is under greater obligation to ensure that the benefits outweigh the harm.
Several factors complicate the demonstration of benefits of EFM as a screening test. There is no consensus regarding a protocol of fetal surveillance for low-risk patients who account for approximately 25% of intrapartum fetal asphyxia. Moderate and severe asphyxia cannot be prevented when asphyxia1 exposure has occurred before labor or before the onset of fetal surveillance. Prediction of intrapartum fetal asphyxia cannot occur when the quality of the record does not permit interpretation. Interpretation of predictive fetal heart rate patterns cannot occur unless the record is consistently and carefully scored. Prediction of most cases of intrapartum fetal asphyxia on the basis of fetal heart rate patterns is possible but difficult. Because the goal of intrapartum fetal surveillance is the prevention of moderate and severe fetal asphyxia, prediction must be achieved before fetal decompensation. Prediction must occur before absent baseline fetal heart rate variability is evident in the record, which is uniformly associated with cerebral dysfunction and, in some cases, brain damage. The possibility of fetal asphyxia must be considered when, within a 1-hour window of recording, there are two or more cycles of minimal baseline fetal heart rate variability and two or more cycles of late or prolonged decelerations or both. Because approximately 9 of 10 predictive fetal heart rate patterns are false-positive, supplementary tests to confirm the diagnosis and to identify false-positives to prevent unnecessary intervention are essential. Until such time as additional fetal assessment tests are validated, blood gas and acid-base assessment of fetal blood can provide a definitive diagnosis and identify false-positive predictions. References 1. Alberman E, Blatchley N, Botting 8, et al: Medical causes on still birth certificates in England and Wales: Distribution and results of hierarchial classification tested by the Office of National Statistics. Br J Obstet Gynaecol 104:1043-1049, 1997 2. Ball RH, Espinoza MI, Parer JT: Regional blood flow in asphyxiated fetuses with seizures. Am J Obstet Gynecol 170:156-161, 1994 3. Ball RH, Parer JT, Caldwell LE, et al: Regional blood flow and metabolism in ovine fetuses during severe cord occlusion. Am J Obstet Gynecol 171:1549-1555, 1994 4. Bax M, Nelson KB: Birth asphyxia: A statement. Dev Med Child Neurol 35:10021004, 1993 5. Burke CJ, Tannenberg AE: Prenatal brain damage and placental infarction, an autopsy study. Dev Med Child Neurol37555-562, 1995 6. Chang A, Sahota DS, Reed NN, et al: Computerized fetal heart rate analysis in labor-ffect of sampling rate. Eur J Obstet Gynecol Reprod Biol 59A2.5-129, 1995 7. Cohn HE, Sacks EJ, Heymann MA, et al: Cardiovascular response to hypoxemia and acidemia in fetal lambs. Am J Obstet Gynecol 120:817-824, 1974 8. deHaan HH, vanReempts JLH, Vles JSH, et al: Effects of asphyxia on the fetal lamb brain. Am J Obstet Gynecol 69:1493-1501, 1993 9. deHaan HH, G u m AJ, Gluckman PD: Experiments in perinatal brain injury: What have we learnt? Prenat Neonat Med 1:1&25, 1996 10. Ellis WG, Goetzman BW, Lindenberg J A Neuropathologic documentation of prenatal brain damage. Am J Dis Child 142858466,1988
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11. Field DR, Parer JT, Auslander RA, et al: Cerebral oxygen consumption during asphyxia in fetal sheep. J Dev Physiol 14:131-137, 1990 12. Gaffney G, Squire W,Johnson A, et al: Clinical association of prenatal ischemic white
matter injury. Arch Dis Child 70:F101-F106, 1994 13. Gunn AJ, Parer JT,Mallard EC, et al: Cerebral histological and electrophysiological changes after asphyxia in fetal sheep. Pediatr Res 31:48-91, 1992 14. Holmquist J?, Svenningsen NW, Ingermarsson I: Neurodevelopmental outcome and electronic fetal heart rate monitoring in a neonatal intensive care population. Acta Obstet Gynecol Scand 63527432,1984 15. Hon EH: The electronic evaluation of the fetal heart rate: Preliminary report. Am J Obstet Gynecol 751215-1230, 1958 16. Hon EH, Quilligan EJ: Electronic evaluation of fetal heart rate: Further observations on "pathologic" fetal bradycardia. Clin Obstet Gynecol 1:145-167, 1968 17. Iida K, Takashima S, Taken& Y Neuropathologic study of newborns with prenatal onset of leukomalacia. Pediatr Neurol 9:45-48, 1993 18. Ikeda T, Murata Y, Quilligan EJ, et al: Physiological and histological changes in near term fetal lamb exposed to asphyxia by partial umbilical cord occlusion. J SOCGynecol Invest 3:256A, 1996 19. Itskovitz J, LaGamma EF, Rudolph AM: Effect of cord compression of fetal blood flow distribution and O2delivery. Am J Physiol252:HlO&H109, 1987 20. James LS, Morishimo HO, Daniel SS, et al: Mechanism of late decelerations of the fetal heart rate. Am J Obstet Gynecol 113578, 1972 21. Jensen A, Roman C, Rudolph A M Effects of reducing uterine blood flow on fetal blood flow distribution and oxygen delivery. J Dev Physiol 15309-323, 1991 22. Jensen A, Lang U: Fetal circulatory responses to arrest of uterine blood flow in sheep: Effects of chemical sympathectomy. J Dev Physiol 1775-86, 1992 23. Low JA, Galbraith RS, Muir DW, et al: Motor and cognitive deficits after intraparturn fetal asphyxia in the mature infant. Am J Obstet Gynecol 158:356-361, 1988 24. Low JA, Robertson DM, Simpson LL: Temporal relationships of neuropathology due to perinatal asphyxia. Am J Obstet Gynecol 160:608-614, 1989 25. Low JA, S i p s o n LL, Ramsay D A The clinical diagnosis of asphyxia responsible for brain damage in the human fetus. Am J Obstet Gynecol 16711-15,1992 26. Low JA, Galbraith RS, Muir DW, et a1 Mortality and morbidity after intraparturn asphyxia in the preterm fetus. Obstet Gynecol 8057-61, 1992 27. Low JA, Panagiotopoulos C, Derrick EJ: Newborn complications after intrapartum asphyxia with metabolic acidosis at term. Am J Obstet Gynecol 170:1081-1087, 1994 28. Low JA, Panagiotopoulos C, Derrick EJ: Newborn complications after intrapartum asphyxia with metabolic acidosis in the preterm fetus. Am J Obstet Gynecol 172:805810, 1995 29. Low JA, Simpson LL, Tonni G, et a1 Limitations in the clinical prediction of intrapartum fetal asphyxia. Am J Obstet Gynecol 172:801-804, 1995 30. Low JA Intrapartum fetal asphyxia: Definition, diagnosis and classification. Am J Obstet Gynecol 176:957-959, 1997 31. Low JA, Lindsay BG, Derrick EJ: Threshold of metabolic acidosis associated with newborn complications. Am J Obstet Gynecol 1771391-1394, 1997 32. Low JA, Victory R, Derrick EJ: Predictive value of electronic fetal monitoring for intrapartum fetal asphyxia with metabolic acidosis. Obstet Gynecol, in press 33. Mallard EC, Gunn AJ, Williams EJ, et al: Transient umbilical cord occlusion causes hippocampal damage in the fetal sheep. Am J Obstet Gynecol 1671423-1430, 1992 34. Mallard EC, Williams CE, Gunn AJ, et al: Frequent episodes of brief ischemia sensitize the fetal sheep brain to neuronal loss and induce striatal injury. Pediatr Res 33:61-65, 1993 35. Mallard EC, Waldvogel HJ, Williams CE, et al: Repeated asphyxia causes loss of striatal projection neurons in the fetal sheep brain. Neuroscience 65:827-836, 1995 36. Martin CB: Regulation of the fetal heart rate and genesis of fetal heart rate patterns. Semin Perinatol2:131-146, 1978 37. Mueller-Heubach E, Myers RE, Adamson K Fetal heart rate and blood pressure during prolonged partial asphyxia in the rhesus monkey. Am J Obstet Gynecol137:48-52,1980
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38. Murata Y, Martin CB, Ikenoue T, et al: Fetal heart rate accelerations and late decelerations during the course of intrauterine death in chronically catheterized rhesus monkeys. Am J Obstet Gynecol 144.21%223, 1982 39. Myers RE: Two patterns of perinatal brain damage and their conditions of occurrence. Am J Obstet Gynecol 112246376, 1972 40. National Institute of Child Health and Human Development Research Planning Workshop: Electronic fetal heart rate monitoring: Research guidelines for interpretation. Am J Obstet Gynecol 177:1385-1390, 1997 41. National !kxening Committee: Annual Report. Milton, Keynes, National Screening Committee, 1998 42. Neilson J P EFM alone vs intermittent auscultation in labor [revised 04 May 19941. In Keirse MJNC, Renfrew MJ, Neilson JP, et a1 (eds): Pregnancy and Childbirth Module. The Cochrane Pregnancy and Childbirth Database. The Cochrane Collaborative, Issue 2. Oxford, Update Software, 1995 43. Nelson KB, Ellenburg J H Antecedents of cerebral palsy: Multivariate analysis of risk. N Engl J Med 3158146,1986 44. Nicolaides KH, Economides DL, Soothill PW: Blood gases, pH and lactate in appropriate and small for gestational age fetuses. Am J Obstet Gynecol 161:9961001, 1989 45. Nicolini V, Nicolaides KH, Fisk N: Limited role of fetal blood sampling in prediction of outcome in intrauterine growth retardation. Lancet 336:76%777,1990 46. Painter MJ, Scott M, Hirsch RF,et al: Fetal heart rate patterns during labour: Neurologic and cognitive development at six to nine years of age. Am J Obstet Gynecol 159854858, 1988 47. Paneth N, Bommarito M, Stricker J: Electronic fetal monitoring and later outcome. Clin Invest Med 16159-165, 1993 48. Pardi G, Cetin I, Marconi AM, et a1 Diagnostic value of blood sampling in fetuses with growth retardation. N Engl J Med 328:692-696, 1993 49. Parer JT, Krueger TR, Harris JL: Fetal oxygen consumption and mechanisms of heart rate response during artificially produced late decelerationsof fetal heart rate in sheep. Am J Obstet Gynecol 136478, 1980 50. Peeters LL, Sheldon RD, Jones MD, et a1 Blood flow total organs as a function of arterial oxygen content. Am J Obstet Gynecol 135637446, 1979 51. Pelowski A, Finer NN: Birth asuhvxia in the term infant. In Sinclair 1, Lucev I (eds): Effective Care of the New6om Infant. Oxford, Oxford University PASS,1692, pp 263-266 52. Quilligan EJ, Paul RH:Fetal monitoring: Is it worth it? Obstet Gynecol45:96100, 1975 53. Ran& JE, Windle WF: Brain damage in the monkey Mucacca mulatta by asphyxia neonatorum. Exp Neurol 1:130-154,1959 54. Reid DL, Parer JT, Williams K, et al: Effects of severe reduction in maternal placental blood flow in blood flow distribution in the sheep fetus. J Dev Physiol1518>188,1991 55. Richardson BS, Patrick JE, Abduljabber H Cerebral oxidative metabolism in fetal sheep: Relationship to electrocortical state. Am J Obstet Gynecol 153:426-431, 1985 56. Richardson BS, Rurak D, Patrick JE, et al: Cerebral oxidative metabolism during sustained hypoxemia. J Dev Physiol 11:37-43, 1989 57. Richardson BS, Carmichael L, Homan J, et al: Cerebral oxidative metabolism in fetal sheep with prolonged and graded hypoxemia. J Dev Physiol 10:7743, 1993 58. Rosen MG, Dickinson JC: The paradox of electronic fetal monitoring: More data may not enable us to predict or prevent infant neurolonic morbiditv. Am I Obstet Gvnecol 168:745-751, 1995 59. Stewart-Brown S. Farmer A Screeninp; could seriouslv damaze vour health. BMI 314533, 1997 60. Sureau C, Charmine J, Michelon 8: Le probleme due rhythme cardiaque foetal Difficulties &interpretation, solutions techniques. Gynecol Obstet (Paris) 69:259-286, 1970 61. Tiig P, Yamaguchi S, Backer JD,et al: Hypoxic-ischemic cerebral necrosis in midgestational sheep fetuses: Physiopathologiccorrelations. Exp Neurol 80:237-245, 1983 62. Uzan S, Fouillot JP,Sureau C: Computer analysis of FHR patterns in labour. In Spencer JAD (ed): Fetal Monitoring. Tuxbridge, Wells, CHI', 1989, pp 159-164 63. VanGeijn H, Dekker G, deVries J, et al: Fetal heart rate patterns during labor. In
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VanGeijn Jp, Copray FJA (eds):A Critical Appraisal of Fetal Surveillance. Amsterdam, Elsevier, 1994, pp 238-270 64. Victory R, Derrick EJ, Low J A Methodological issues in electronic fetal heart rate monitoring. J SOCGynaecol Invest 5:169A, 1998 65. Vintzileos AM, Nochimson DJ, Guzman ER, et al: Intrapartum electronic fetal heart rate monitoring versus intermittent auscultation: A meta-analysis. Obstet Gynecol 85149-155, 1995 66. Williams CE, Gum AJ, Mallard EC, et ak Outcome after ischemia in the developing sheep brain: An electroencephalographicand histological study. Ann Neurol 3 1 : l l P 121, 1992
Address reprint requests to James A. Low, MD Department of Obstetrics and Gynaecology Watkins 3 Kingston General Hospital Kingston, Ontario, Canada K7L 2V7
0889-8545/99 $8.00
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INTRAPARTUM FETAL SURVEILLANCE Is It Worthwhile? James A. Low, MD
Screening in an attempt to prevent disease is attractive in comparison with the traditional medical model of reacting to disease. Prevention avoids morbidity and mortality and offers a way of reducing expensive medical care. Although for many years screening has been considered to be harmless, a growing body of evidence suggests that screening can harm individuals, particularly via the adverse effects of false-positive and false-negative results.59The skepticism regarding the benefits of screening has been highlighted by the first annual report of the National Screening Committee in the United Kingdom.4l That report concluded that only 4 of 100 screening programs in clinical practice met the criteria for quality or evidence of effectiveness. Two questions must be addressed regarding the current surveillance of the fetus during labor: (1)the clinical problem of whether the significance of intraparturn fetal asphyxia justifies intervention to provide fetal surveillance, and (2) the fetal surveillance problem of whether the benefits outweigh the harm. CLINICAL PROBLEM
Understanding of the association between fetal asphyxia and brain damage is based on research in the fetal monkey and lamb. Studies of From the Departments of Obstetrics and Gynaecology and Paediatrics, Queen’s University, Kingston, Ontario, Canada
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global asphyxia9,3z, 35, 53 and cerebral ischemia3" have confirmed that exposure of more than 10 minutes is associated with brain damage. Studies of partial asphyxias,13, 39, have demonstrated that sustained partial asphyxia of 1 to 3 hours may or may not be associated with brain damage. The key to the occurrence of brain damage is severe fetal metabolic acidosis and cardiovascular decompensation with systemic hypotension. Clinical studies require a definition and diagnostic criteria of potentially significant fetal asphyxia. A task force set up by the World Federation of Neurology Group defined asphyxia as a condition of impaired gas exchange leading, if it persists, to progressive hypoxemia and hypercapnia.4 According to this definition, asphyxia may occur in a transient fashion, which although of physiologic interest, has no pathologic significance. Pathology owing to asphyxia is caused by progressive hypoxemia leading to tissue oxygen debt with accumulation of fixed acids and a metabolic acidosis; therefore, the following addition has been proposed for the definition of potentially significant intraparturn fetal asphyxia3? Fetal asphyxia is a condition of impaired blood gas exchange leading, if it persists, to progressive hypoxemia and hypercapnia with a metabolic acidosis.
This definition serves as a reminder that the definitive diagnosis of asphyxia requires a blood gas and acid-base assessment. The important question for fetaI asphyxia is the threshoId of metabolic acidosis beyond which fetal morbidity and mortality may occur. A series of clinical studiesZ7, z8, 31 have demonstrated that the threshold of metabolic acidosis beyond which moderate and severe newborn complications and particularly newborn encephalopathy begin to occur is an umbilical artery base deficit greater than 12 mmol/L. The frequency of moderate and severe newborn complications in relation to the degree of metabolic acidosis is summarized in Table 1. There is a threshold of asphyxia1 exposure expressed by umbilical artery base deficit beyond which some newborns may and some newborns may not have evidence of brain dysfunction or other organ system complications. Brain dysfunction may be reversible and the clinical manifestations transient. In other cases, particularly those with severe newborn encephalopathy, brain damage may occur and account for subsequent motor
Table 1. FREQUENCY OF MODERATE OR SEVERE NEWBORN COMPLICATIONS IN RELATION TO DEGREE OF METABOLIC ACIDOSIS AT DELIVERY ~~
~
~~
Metabolic Acidosis Umbilical Artery Base Deficit
~~
Newborn Complications Moderate or Severe
12-16 -ol/L
10%
>16 mmol/L
40%
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and cognitive deficits. The occurrence of motor and cognitive deficits after biochemically confirmed intrapartum fetal asphyxia has been exam26 Many children demonstrated ined in term and preterm ne~borns.2~. normal motor and cognitive development at 1 year of age. Nevertheless, in both studies, there was a significant increase in the occurrence of motor and cognitive deficits or brain damage in early neonatal deaths after fetal asphyxia in the term and preterm newborns. These clinical studies emphasize that despite the occurrence of newborn and long-term morbidity after intrapartum fetal asphyxia, a large number of infants do not exhibit evidence of newborn brain dysfunction or subsequent clinical manifestations of brain damage. Current understanding of the variable outcome after fetal asphyxia is based on the concept of fetal cardiovascular compensation developed in research studies in the fetal lamb. The effect of fetal asphyxia owing to maternal hyp~xemia,~,56, 57 reduced uteroplacental blood flow? 21, 30, 54 and cord o c c l ~ s i o non ~ , ~fetal ~ cardiovascular function has been examined. There has been a remarkable consistency of the fetal cardiovascular response in these different models. The initial response to an asphyxia1 exposure is an increase of arterial pressure owing to increased systemic vascular resistance mediated by the autonomic nervous system.22There is a redistribution of cardiac output, with decreased blood flow to the lungs, kidney, gastrointestinal system, and body and a centralization of circulation with increased blood flow to the brain, heart, and adrenals. This cardiovascular response is important to the integrity of the central nervous system. Cerebral oxygen requirements are reduced with an increase of highvoltage electrocortical Cerebral oxygen metabolism is maintained because of a combination of increased cerebral blood flow and oxygen extraction. A classification of the severity of an asphyxial exposure is required to predict the long-term outcome in the child. The significance of fetal asphyxia depends on several factors, including the degree, duration, and nature (continuous or intermittent) of the asphyxial exposure and the quality of the fetal cardiovascular response. In the clinical setting, a measure of the degree of metabolic acidosis confirms that an asphyxial exposure has occurred; however, information regarding the duration and nature of the exposure and the fetal cardiovascular response is generally not available. A classification of the severity of intrapartum fetal asphyxia has been proposed by determining the short-term outcome as expressed by newborn encephalopathy and other newborn organ system complications (Table 2).3O This classification is based on the evidence that early-onset newborn encephalopathy is the best single predictor of longterm outcome. In a review of five studies of term newborns, Pelowski and FineP reported a good outcome for newborns with minor newborn encephalopathy, whereas the risk of death or severe disability was 5.6% and 20% for newborns with moderate encephalopathy and 60% and 72% for newborns with severe encephalopathy, respectively. Cardiovascular, respiratory, and particularly renal complications provide a further indi-
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Table 2. CLASSIFICATIONOF INTRAPARTUMFETAL ASPHYXIA
Degree of Asphyxia ~
Mild Moderate Severe
Metabolic Acidosis at Delivery*
+ + +
Cardiovascular, Respiratory, and Renal Complications
Encephalopathy Minor ~~
*
Moderate
Severe
Minor
Moderate to Severe
f
+
f
+
+
+
= present; & = present or absent. ‘Umbilical artery base defiats 212 mmol/L. From Low JA: Intraparturn fetal asphyxia: Definition, diagnosis and classification. Am J Obstet Gynecol 176:957-959, 1997; with permission.
cation of the severity of the asphyxial exposure in both term and preterm newborns. Evidence is now available to define the magnitude of the clinical problem of intrapartum fetal asphyxia. Routine blood gas and acid-base assessment of umbilical artery blood at delivery have demonstrated an umbilical artery base deficit of greater than 12 mmol/L in 2% and of greater than 16 mmol/L in 0.5%of the total population. Table 3 summarizes the clinical problem based on the current understanding of the occurrence of moderate and severe newborn encephalopathy in these categories of metabolic acidosis and of subsequent death or severe disability in relation to the severity of newborn encephalopathy. Moderate or severe asphyxia occurs in 3 to 4 per 1000 births, of which approximately 1 per 1000 has evidence of brain damage. INTRAPARTUM FETAL SURVEILLANCE
The goal of intrapartum fetal surveillance is to reduce the incidence of fetal asphyxial exposure and to prevent moderate and severe asphyxia. Because intrapartum fetal asphyxia is usually partial and often Table 3. MAGNITUDE OF THE CLINICAL PROBLEM OF INTRAPARTUM FETAL ASPHYXIA ~
~
~~
Outcome per 1000 Births Umbilical Artery Base Deficit Event
Asphyxia1 exposure Mild Moderate/severe Asphyxia with brain damage
12-16 mmoUL
>16 mmoUL
15.0 13.5
5.0 3.0 2.0
\
1
J
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intermittent, fetal compensation may be satisfactory for some time (hours). This interval provides a window of opportunity during which the occurrence of an asphyxial exposure can be confirmed, and, when appropriate, intervention can be initiated before the threshold of decompensation has been reached. A clinical paradigm for the prediction and diagnosis of intrapartum fetal asphyxia emerged in the 1960s as a result of three developments: clinical risk scoring, electronic fetal heart rate monitoring (EFM), and microelectrodes permitting fetal blood gas and acid-base assessment. It was proposed that clinical risk scoring would identify pregnancies at risk for intraparturn fetal asphyxia, that continuous EFM of risk pregnancies would identify the fetus experiencing an asphyxial exposure, and that blood gas and acid-base assessment of fetal blood would confirm the fetal asphyxia with a developing metabolic acidosis. Clinical Risk Scoring
Two studies have highlighted the limitations of clinical risk 29 Fetal exposure to asphyxia occurs in pregnancies with no clinical risk factors. This observation was made in 23% of pregnancies with a potentially significant metabolic acidosis at delivery and in 40% of perinatal deaths with postmortem evidence of brain damage owing to antepartum or intrapartum fetal asphyxia. In cases in which clinical risk factors were present, risk was determined by a wide range of complications, with no single risk factor demonstrating a strong association with intrapartum fetal asphyxia. The positive predictive value for antepartum and intrapartum risk factors was 3%, with a low predictive value for each individual risk factor. Clinical risk scoring has a major problem of false-positive prediction of intrapartum fetal asphyxia. Clinical risk scoring is a valuable method of assessment of the obstetric patient and her pregnancy; however, clinical risk scoring is of limited predictive value for intrapartum fetal asphyxia. There are no low-risk pregnancies for intraparturn fetal asphyxia. Because of the major problem of false-positive findings, at-risk pregnancies require supplementary tests to justify intervention for suspected fetal asphyxia. Electronic Fetal Heart Rate Monitoring
Fetal heart rate observations began in the nineteenth century, whereas EFM was developed in the twentieth century.l5,6o Despite this long history, the value of intermittent fetal heart rate auscultation and continuous EFM in the prediction of intrapartum fetal asphyxia has yet to be established. The evidence to date indicates that EFM has been associated with
a reduction in the number of intraparturn fetal deaths5' 65; however, intrapartum deaths continue to occur. A national study of stillbirths in England and Wales between 1993 and 1995 reported that 10% of stillbirths occurred in the intraparturn period, most of which were attributed to asphyxia.' Limited evidence suggests an association between abnormal fetal heart rate patterns and neurologic abnormality in surviving ~hildren.'~, 46 In a retrospective study of children with cerebral palsy, Rosen and D i c k i n s ~ nfailed ~ ~ to find a consistent fetal heart rate pattern that would predict brain injury. It was concluded that these findings should not be surprising because most brain damage occurs outside the intraparturn period. Well-designed randomized clinical trials have been proposed to minimize selection bias and to determine the true risks and benefits of a medical intervention. No randomized clinical trials have compared no fetal heart rate surveillance with intermittent fetal heart rate auscultation. The value of EFM is increasingly questioned because of recently reported randomized trials of this test?" EFM has failed to provide consistent evidence of decreased fetal or newborn morbidity or mortality. Two confounding factors may be the numbers in the study population and the modified clinical management in study protocols. Nevertheless, the trials to date have made an important contribution, demonstrating that EFM has been associated with unnecessary intervention, with an increased incidence of cesarean delivery for fetal distress and dystocia, operative delivery, and general anesthesia." These findings emphasize the need for a better understanding of the predictive limitations of EFM. Laboratory evidence indicates that fetal heart rate assessment should be of value in the prediction of fetal asphyxia. Studies in the fetal lamb have demonstrated a relationship between late decelerations and fetal hypoxemia and metabolic acidosis. Late decelerations have been shown to occur when fetal oxygen tension decreases below a critical level. The interval between the onset of the contraction and the onset of the deceleration reflects the time necessary for the fetal oxygen tension to fall below this threshold.20,37, 38 Late decelerations in relation to fetal hypoxemia in a previously normoxic fetus are the result of chemoreceptor-initiated reflex bradycardia, which can be blocked by atropine, whereas in the previously hypoxic fetus, the bradycardia may be the result of a direct effect on the myocardium.3'jr49 It has been difficult to provide evidence that the benefits of EFM outweigh the harm as a test of fetal assessment. Three factors may account for these equivocal results: Asphyxia may occur before the onset of labor. Methodologic issues may exist in regards to the assessment protocol and fetal heart rate interpretation. Limitations may apply to the predictive value of fetal heart rate patterns.
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Anteparturn Fetal Asphyxia
Fetal asphyxia may occur in the antepartum period. The significance of antepartum fetal complications including asphyxia was implied in the data from the National Collaborative Perinatal Project, which determined that when all principal risk factors present by the time that labor began were considered, 5% of the population at highest risk contributed to 34% of the cases of cerebral pal~y.4~ The occurrence of antepartum brain damage has been demonstrated in postmortem studies. Studies of stillbirths and early neonatal deaths indicate that a sublethal asphyxial exposure in the preterm and term fetus prior to the onset of labor can cause brain damage with characteristic neuropathologic findings.5,10,12,17,24 Recent antepartum cordocentesis studies have confirmed the occurrence of antepartum fetal asphyxial exposure. Some fetuses, particularly those believed to be growth-retarded, have demonstrated hypoxemia, hypercapnia, and metabolic acidosis prior to the onset of labor.” a5, Nevertheless, there is no information on the prevalence of biochemically confirmed fetal asphyxia in the antepartum period. In the absence of a precise diagnosis, the contribution of antepartum fetal asphyxia to brain damage and neurodevelopmental disability has not been established. This limitation may complicate intrapartum fetal assessment because the assessment during labor may reflect events occurring prior to the onset of labor. Methodologic Issues
Numerous factors may affect the appropriate use of EFM. These include the duration of the assessment, the quality of fetal heart rate data, the classification and interpretation of fetal heart rate variables, and the interpretation of the fetal heart rate record. Ideally, fetal intrapartum surveillance should begin with onset of labor. With the exception of the induction of labor, this timing is rarely achieved. Thus, intrapartum fetal asphyxial exposure may occur before fetal assessment is initiated. When fetal surveillance begins, the duration of the record must be sufficient to permit interpretation of the pattern of fetal heart rate behavior. The quality of the fetal heart rate data must be adequate for interpretation. In 1958, Hon15 reported that electronic techniques provided a more accurate indication of fetal heart rate than was possible with intermittent auscultation. This is true in the classification of baseline fetal heart rate variability and decelerations. The quality of the recording must also be adequate for interpretation. Ultrasound fetal heart rate signal and the tocodynometer have provided an attractive noninvasive option; however, in some cases, the fetal heart rate signal and particularly the uterine contraction waveform may not be satisfactory, in which case a scalp electrode and intrauterine catheter are required.
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Differences of classification criteria remain, particularly for decelerations. In the classification of late decelerations, some clinicians have given first priority to the timing of the nadir of the deceleration, whereas others have emphasized the waveform. In interpretation of the waveform, both the onset to the nadir16 and the residual component of the waveform have been examined.62Efforts to quantify decelerations are continuing."63 Until a consensus is developed, as recently recommended, interpretation criteria should be clearly defined and consistently used.40 Although progress has been made in regards to computer-based interpretation of fetal heart rate records, with few exceptions, clinical records are read visually. The limited interobserver reliability for visual A interpretation of fetal heart rate patterns has been well-d0cumented.4~ recent study at the author's center demonstrated the following good-tofair interobserver Kappa values: baseline fetal heart rate, 0.70; baseline fetal heart rate variability, 0.55; fetal heart rate accelerations, 0.56; variable decelerations, 0.46; and late or prolonged decelerations, 0.57. This limited interobserver reliability of individual fetal heart rate variables can be offset by scoring fetal heart rate patterns. In 20 fetal heart rate records, the classification of fetal heart rate patterns in 1 hour of recording was similar between two observers." The interpretation of fetal heart rate patterns based on variables that have an association with potentially significant metabolic acidosis requires an examination of the fetal heart rate record over time. The record should be scored in 10-minute epochs (cycles). Determination of the pattern requires careful scoring of a number of cycles, which, in most cases, can be achieved with six cycles representing 1 hour of the fetal heart rate record. Predictive Fetal Heart Rate Variables
The fetal heart rate variables associated with intrapartum fetal asphyxia with a potentially significant metabolic acidosis were determined in a matched case-control study performed by the author and his colThe study population included 71 fetuses in the asphyxia group (umbilical artery base deficit >16 mmol/L) and 71 in the control group (umbilical artery base deficit <8 mmol/L). The severity of the asphyxia1 exposure in the asphyxia group was classified as mild (n = 41), moderate (n = 17), or severe (n = 13). Each fetal heart rate record was scored in 10-minute cycles over the last 4 hours of labor. The baseline fetal heart rate variables scored included baseline fetal heart rate and baseline fetal heart rate variability. The periodic fetal heart rate variables scored included accelerations and variable, early, late, and prolonged decelerations. Three fetal heart rate variables (baseline fetal heart rate, variable, and early decelerations) did not discriminate between the asphyxia and
INTRAPARTUM FETAL SURVEILLANCE
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control groups. One fetal heart rate variable (spontaneous accelerations) had an association with the control group. Three fetal heart rate variables (baseline fetal heart rate variability, late decelerations, and prolonged decelerations)had a significant association with the asphyxia group during the last hour of the fetal heart rate record; however, no single fetal heart rate variable occurred in all asphyxia cases, and each fetal heart rate variable occurred in the absence of fetal asphyxia. Each predictive fetal heart rate variable may occur in one cycle or two or more cycles and may occur independently or in combination with another fetal heart rate variable; therefore, fetal heart rate patterns based on the findings in six 10-minute cycles of recording are required to determine the predictive value of repetitive combined fetal heart rate variables for asphyxia. The fetal heart rate patterns examined in the author’s study were absent baseline variability, usually with repetitive cycles (two or more) of late or prolonged decelerations; repetitive cycles (two or more) of minimal baseline fetal heart rate variability and late or prolonged decelerations; repetitive cycles (two or more) of either minimal baseline fetal heart rate variability or late or prolonged decelerations; and one cycle of either minimal baseline fetal heart rate variability or late or prolonged decelerations. Absent baseline fetal heart rate variability with repetitive late or prolonged decelerations occurred principally in the asphyxia group. In the remaining cases, the association with asphyxia decreased with decreasing frequency of cycles of minimal baseline variability and late or prolonged decelerations or both. The sensitivity of fetal heart rate patterns is outlined in Figure 1. Fetal heart rate patterns with absent baseline variability identified 17% of the asphyxia group and 36% of the moderate and severe asphyxia group. The sensitivity increased to 93% with the addition of less specific patterns. The predictive value of fetal heart rate patterns is outlined in Figure 2. Fetal heart rate patterns with absent baseline variability are most specific, with occasional false-positive findings. The remaining patterns have a low positive predictive value. The prediction of fetal asphyxia by fetal heart rate patterns is possible but difficult. The prediction of moderate and severe asphyxia, that is, after fetal cardiovascular decompensation has occurred, is not consistent with the goal of intrapartum fetal monitoring, thus prediction cannot wait for absent baseline fetal heart rate variability. The possibility of asphyxia must be considered when there is a 1-hour window with two or more cycles of minimal baseline variabiIity and late or prolonged decelerations or both. The potential for unnecessary intervention is great using these criteria. Because intrapartum fetal asphyxia is an infrequent event and because fetal heart rate patterns are not specific, there are a large number of false-positive fetal heart rate patterns.
734
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100
4-
c
a,
60-
e
a, R
40-
20
-
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FHR Pattern FHR Variability Absent (cycles)
I
2
+
3
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-
>I 72
52
I
and
and
or
or
52
52
52
I
Minimal (cycles)
Late & prolonged
+
Decelerations
(cycles)
Figure 1. Fetal heart rate patterns-sensitivity. A sensitivity for prediction of fetal asphyxia of 93% can be achieved if all fetal heart rate patterns with minimal baseline variability and late or prolonged decelerations are included. Open bars = mild and moderatelsevere asphyxia; and solid bars = moderatelsevereasphyxia.
Supplementary Tests
If EMF is to be used as a screening test for intrapartum fetal asphyxia, predictive fetal heart rate patterns require supplementary tests to confirm the diagnosis of fetal asphyxia and to identify false-positive tests to avoid unnecessary intervention. A number of supplementary tests are currently being assessed, including fetal vibroacoustic stimulation, the ST segment and PR interval of the fetal electrocardiogram, fetal pulse oximetry fetal pH electrode, and near-infrared spectroscopy. Although potential benefits have been reported, particularly in the identification of false-positive fetal heart rate patterns, the clinical value of these tests remains to be determined. A fetal blood gas and acid-base assessment with evidence of a metabolic acidosis is the gold standard for the diagnosis of fetal asphyxia. The occurrence or exclusion of intrapartum fetal asphyxia can be confirmed by a blood gas and acid-base assessment of umbilical vein and artery blood at delivery without compromising either the gravida or fetus. If moderate and severe intrapartum fetal asphyxia are to be prevented, the occurrence of asphyxia1 exposure with a developing metabolic acidosis must be confirmed before delivery. A scalp sample of fetal
LNTRAI'ARTUM FETAL SURVEILLANCE
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100
80 c
c
al
eal
a
-
60,40-
20
I
0
FHR Pattern
I
+
2
+
3
+
4
FHR Variability Absent (cycles) Minimal (cycles) Late & prolonged Decelerations
5I
and 32
52
52
and
or
52
or I
Figure 2. Fetal heart rate patterns-predictivevalue. False-positiveprediction is a frequent occurrence with fetal heart rate patterns including minimal baseline variability and late or prolonged decelerations. Open bars = true-positive; solid bars = false-positive.
blood for a blood gas and acid-base assessment is currently the only test that can confirm this diagnosis or identify false-positive predictive tests. SUMMARY
Potentially sigruficant intrapartum fetal asphyxia occurs in approximately 20 per 1000 births. Moderate and severe fetal asphyxia exposure with newborn morbidity occurs in 3 to 4 per 1000 births, with brain damage and subsequent disability in at least 1per 1000 births. Although the prevalence of moderate and severe asphyxia is modest, prevention is important because of the serious implications of this complication to the child, family, and society. Because of the limited predictive value of clinical risk factors, the interpretation of patterns in a fetal heart rate record has become the primary screening test for intrapartum fetal asphyxia. Despite extensive clinical experience and numerous clinical trials, the benefits of EFM as a screening test have not been established, and harm may occur owing to unnecessary intervention. This observation raises serious ethical issues. When an intervention is initiated by the clinician rather than the patient, the clinician is under greater obligation to ensure that the benefits outweigh the harm.
Several factors complicate the demonstration of benefits of EFM as a screening test. There is no consensus regarding a protocol of fetal surveillance for low-risk patients who account for approximately 25% of intrapartum fetal asphyxia. Moderate and severe asphyxia cannot be prevented when asphyxia1 exposure has occurred before labor or before the onset of fetal surveillance. Prediction of intrapartum fetal asphyxia cannot occur when the quality of the record does not permit interpretation. Interpretation of predictive fetal heart rate patterns cannot occur unless the record is consistently and carefully scored. Prediction of most cases of intrapartum fetal asphyxia on the basis of fetal heart rate patterns is possible but difficult. Because the goal of intrapartum fetal surveillance is the prevention of moderate and severe fetal asphyxia, prediction must be achieved before fetal decompensation. Prediction must occur before absent baseline fetal heart rate variability is evident in the record, which is uniformly associated with cerebral dysfunction and, in some cases, brain damage. The possibility of fetal asphyxia must be considered when, within a 1-hour window of recording, there are two or more cycles of minimal baseline fetal heart rate variability and two or more cycles of late or prolonged decelerations or both. Because approximately 9 of 10 predictive fetal heart rate patterns are false-positive, supplementary tests to confirm the diagnosis and to identify false-positives to prevent unnecessary intervention are essential. Until such time as additional fetal assessment tests are validated, blood gas and acid-base assessment of fetal blood can provide a definitive diagnosis and identify false-positive predictions. References 1. Alberman E, Blatchley N, Botting 8, et al: Medical causes on still birth certificates in England and Wales: Distribution and results of hierarchial classification tested by the Office of National Statistics. Br J Obstet Gynaecol 104:1043-1049, 1997 2. Ball RH, Espinoza MI, Parer JT: Regional blood flow in asphyxiated fetuses with seizures. Am J Obstet Gynecol 170:156-161, 1994 3. Ball RH, Parer JT, Caldwell LE, et al: Regional blood flow and metabolism in ovine fetuses during severe cord occlusion. Am J Obstet Gynecol 171:1549-1555, 1994 4. Bax M, Nelson KB: Birth asphyxia: A statement. Dev Med Child Neurol 35:10021004, 1993 5. Burke CJ, Tannenberg AE: Prenatal brain damage and placental infarction, an autopsy study. Dev Med Child Neurol37555-562, 1995 6. Chang A, Sahota DS, Reed NN, et al: Computerized fetal heart rate analysis in labor-ffect of sampling rate. Eur J Obstet Gynecol Reprod Biol 59A2.5-129, 1995 7. Cohn HE, Sacks EJ, Heymann MA, et al: Cardiovascular response to hypoxemia and acidemia in fetal lambs. Am J Obstet Gynecol 120:817-824, 1974 8. deHaan HH, vanReempts JLH, Vles JSH, et al: Effects of asphyxia on the fetal lamb brain. Am J Obstet Gynecol 69:1493-1501, 1993 9. deHaan HH, G u m AJ, Gluckman PD: Experiments in perinatal brain injury: What have we learnt? Prenat Neonat Med 1:1&25, 1996 10. Ellis WG, Goetzman BW, Lindenberg J A Neuropathologic documentation of prenatal brain damage. Am J Dis Child 142858466,1988
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11. Field DR, Parer JT, Auslander RA, et al: Cerebral oxygen consumption during asphyxia in fetal sheep. J Dev Physiol 14:131-137, 1990 12. Gaffney G, Squire W,Johnson A, et al: Clinical association of prenatal ischemic white
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Address reprint requests to James A. Low, MD Department of Obstetrics and Gynaecology Watkins 3 Kingston General Hospital Kingston, Ontario, Canada K7L 2V7