Pediatric Annals

Intrapartum Fetal Surveillance: A Reappraisal

Michael D Berkus, MD; Oded Langer, MD

Abstract

Although sanitation and better septic techniques improved neonatal outcome in the early 190Os, it was not until the middle of the century that any real attention was focused by obstetricians on infant morbidity and mortality. Until that time, the opportunity to intervene if abnormalities were uncovered during delivery were limited to the use of forceps late in the labor process. With the advent of blood banking and antibiotics after World War II, abdominal delivery was safe, and pregnancy could be interrupted at any stage on behalf of the fetus if indicated. As the focus shifted away from maternal survival to fetal wellbeing, improved methods to evaluate the intrauterine environment both before and during labor were sought.

Through the research of Barron,1 Apgar,2 James,3 and others, the primary mechanism of fetal damage during labor was identified as an insufficient supply of oxygen to the fetus secondary to reduction in blood supply in the intravillous space. As hypoxia developed, lactate accumulated, causing swelling of fetal brain cells leading to necrosis, subsequent brain damage, and death. If it were possible to determine when these events occurred, safe techniques existed to deliver the fetus and avoid these adverse events . During the 1950s and early 1960 s Saling,4 Hon and Quilligan,5 and Caldeyro-Barcia6 developed methods to monitor fetal status during labor to detect fetal compromise. Within 10 years of this work, electronic fetal monitoring equipment for intrapartum fetal evaluation became commercially available.

As understanding of fetal physiology and the effects of clinical management on outcome increased, attention shifted from mother to infant. As a result, the cesarean section rate has increased dramatically to respond to the increased recognition of early hypoxic events. The perinatal mortality has shown dramatic reductions from 30 per 1000 to 6 to 8 per 1000 during this same period; however, many other factors have contributed to this improvement, and electronic fetal monitoring may be only a minor element.

No prospective, randomized study has shown electronic fetal monitoring to be superior to older methods of fetal surveillance, including intermittent fetal heart rate auscultation by stethoecope or Doppler, and the presence of meconium-stained amniotic fluid. Yet, electronic fetal monitoring is being used routinely in all hospitals. Why should this be the case?

To determine which fetus is likely to experience a reduction in oxygénation and undergo distress intrapartum, a number of potential indicators have been identified. The presence of meconium-stained amniotic fluid, fetal heart rate characteristics, and fetal acid-base balance have been used to determine fetal status during labor.

MECONIUM-STAINED AMNIOTIC FLUID

A great deal of interest and controversy surround the topic of meconium-stained amniotic fluid. Although meconium-stained amniotic fluid has been viewed as a harbinger of impending or ongoing fetal compromise,7-10 some investigators believe that meconium-stained amniotic fluid is not associated with fetal hypoxia, acidosis, or fetal distress11-14 and may be a normal physiologic event.15 When abnormal fetal heart rate patterns accompany the passage of meconium, there is a 3% to 22.2% perinatal infant mortality rate and a 7% to 50% neonatal morbidity rate.8,16-19 However, several works show no association between meconium-statned amniotic fluid and abnormal tracings, Apgar, and cord pH,7,12,20 or presence of meconium below the vocal cords at delivery.12 Those who have found correlations of meconium-stained amniotic fluid with abnormal fetal heart rate monitoring patterns have not consistently related them to low Apgar scores.8,15

Despite the intuitive view of most obstetricians that thick meconium-stained amniotic fluid is more ominous than thin meconium-stained amniotic fluid, a number of investigators could not demonstrate clear differences in Apgar scores,7-19 fetal heart rate patterns,6 or fetal scalp pH and outcome.16 Conversely, Starks,10 Mitchell,14…

Although sanitation and better septic techniques improved neonatal outcome in the early 190Os, it was not until the middle of the century that any real attention was focused by obstetricians on infant morbidity and mortality. Until that time, the opportunity to intervene if abnormalities were uncovered during delivery were limited to the use of forceps late in the labor process. With the advent of blood banking and antibiotics after World War II, abdominal delivery was safe, and pregnancy could be interrupted at any stage on behalf of the fetus if indicated. As the focus shifted away from maternal survival to fetal wellbeing, improved methods to evaluate the intrauterine environment both before and during labor were sought.

Through the research of Barron,1 Apgar,2 James,3 and others, the primary mechanism of fetal damage during labor was identified as an insufficient supply of oxygen to the fetus secondary to reduction in blood supply in the intravillous space. As hypoxia developed, lactate accumulated, causing swelling of fetal brain cells leading to necrosis, subsequent brain damage, and death. If it were possible to determine when these events occurred, safe techniques existed to deliver the fetus and avoid these adverse events . During the 1950s and early 1960 s Saling,4 Hon and Quilligan,5 and Caldeyro-Barcia6 developed methods to monitor fetal status during labor to detect fetal compromise. Within 10 years of this work, electronic fetal monitoring equipment for intrapartum fetal evaluation became commercially available.

As understanding of fetal physiology and the effects of clinical management on outcome increased, attention shifted from mother to infant. As a result, the cesarean section rate has increased dramatically to respond to the increased recognition of early hypoxic events. The perinatal mortality has shown dramatic reductions from 30 per 1000 to 6 to 8 per 1000 during this same period; however, many other factors have contributed to this improvement, and electronic fetal monitoring may be only a minor element.

No prospective, randomized study has shown electronic fetal monitoring to be superior to older methods of fetal surveillance, including intermittent fetal heart rate auscultation by stethoecope or Doppler, and the presence of meconium-stained amniotic fluid. Yet, electronic fetal monitoring is being used routinely in all hospitals. Why should this be the case?

To determine which fetus is likely to experience a reduction in oxygénation and undergo distress intrapartum, a number of potential indicators have been identified. The presence of meconium-stained amniotic fluid, fetal heart rate characteristics, and fetal acid-base balance have been used to determine fetal status during labor.

MECONIUM-STAINED AMNIOTIC FLUID

A great deal of interest and controversy surround the topic of meconium-stained amniotic fluid. Although meconium-stained amniotic fluid has been viewed as a harbinger of impending or ongoing fetal compromise,7-10 some investigators believe that meconium-stained amniotic fluid is not associated with fetal hypoxia, acidosis, or fetal distress11-14 and may be a normal physiologic event.15 When abnormal fetal heart rate patterns accompany the passage of meconium, there is a 3% to 22.2% perinatal infant mortality rate and a 7% to 50% neonatal morbidity rate.8,16-19 However, several works show no association between meconium-statned amniotic fluid and abnormal tracings, Apgar, and cord pH,7,12,20 or presence of meconium below the vocal cords at delivery.12 Those who have found correlations of meconium-stained amniotic fluid with abnormal fetal heart rate monitoring patterns have not consistently related them to low Apgar scores.8,15

Despite the intuitive view of most obstetricians that thick meconium-stained amniotic fluid is more ominous than thin meconium-stained amniotic fluid, a number of investigators could not demonstrate clear differences in Apgar scores,7-19 fetal heart rate patterns,6 or fetal scalp pH and outcome.16 Conversely, Starks,10 Mitchell,14 and Meis21 found lower Apgar scores, and Starkes4 and Mitchell14 found lower fetal scalp blood pH values with thick meconium-stained amniotic fluid. The consistency of meconium-stained amniotic fluid was not associated with frequency or type of acidemia, low 1- or 5-minute Apgar scores, or newborn neurologic dydfunction.22 Several recent papers that downplay the risks of meconium-stained amniotic fluid consider all grades of meconium as one entity,12,20,21,23 losing the significance of thick meconium-stained amniotic fluid.

Table

TABLE 1Risk for Adverse Outcome

TABLE 1

Risk for Adverse Outcome

Some of this confusion may be explained by the following. The passage of meconium with normal amniotic fluid volume may be a physiological event for the term fetus.15 However, oligohydramnios with decreased placenta! perfusion and chronic fetal hypoxia results in thick meconium-stained amniotic fluid and this could then be associated with adverse outcome indirectly (due to hypoxia) as well as directly from possible aspiration. Furthermore, a developing body of evidence24,25 supports Benirschke's theories that "...it is likely that meconium damages the fetus by acting as a vasoconstrictive agent on the umbilical and superficial vessels."26

We have shown that thick meconium-stained amniotic fluid is an independent risk factor for intrapartum complications, as reflected by increased need for emergent cesarean section and acidotic, umbilical arterial cord pH.27 Moderate or thick meconiumstained amniotic fluid was associated with a greater incidence of adverse neonatal outcome, meconium aspiration syndrome, and significantly more neurological sequelae in that study. This composite group was also at greater risk for abnormal intrapartum monitoring, Apgar scores, and arterial cord pH; and postpartum complications such as sepsis. Finally, logistic regression confirmed the independent contribution of the moderate or thick meconium-stained amniotic fluid to adverse neonatal outcome.

Thick meconium-stained amniotic fluid is the result of meconium passage with decreased amniotic fluid. Relative oligohydramnios occurs with increasing gestational age and is more pronounced as placenta insufficiency causes redistribution of fetal blood flow to vital organs and away from the kidneys and lungs, causing decreased urinary output and egress of respiratory fluid. With decreased perfusion or cord compression, gasping may occur and meconium enters the lungs. Decreased amniotic fluid leads to a higher concentration and retention of passed meconium and increases the opportunity for aspiration. Decreased Jung fluid outflow retards clearance of aspirated meconium from the respiracory tree. Thus, the presence of thick meconiumstained amniotic fluid in early labor should be associated with increasing placenta! insufficiency, meconium aspiration, and adverse neonatal outcome.

Figure 1. Decision tree for treating meconium-stained amniotic fluid.

Figure 1. Decision tree for treating meconium-stained amniotic fluid.

Recently, it has been suggested that there may be a role for meconium-stained amniotic fluid as a direct vasoconstrictor of umbilical and placental vessels.24'26 This has been shown in pathologic studies in which both acute and chronic meconium staining are associated with increased risk of neonatal asphyxia.24 Additionally, 7 of IO infants who had placentas with vascular .necrosis had low Apgar scores and cord pH. Among these 7 was death, a baby with neurological delay, and a case of hydrocephalus secondary to intracranial hemorrhage.25 Attempts to quantify the thickness of meconiumstained amniotic fluid22,28 have used the amount of solid meconium per unit volume, a "meconiumcrit," to determine consistency. Using arbitrary cutoffs, these reports find an excellent correlation (r=0.997) with subjective assessments.

NEONATAL OUTCOME

To determine the impact of meconium-stained amniotic fluid on pregnancy requires a suitable measure of outcome. Previous studies used low Apgar scores to reflect intrapartum asphyxia. However, 1 -minute scores may be low because of vigorous endotracheal suctioning at birth, common with thick meconiumstained amniotic fluid. The scores also can be affected by gestational age, anesthesia, or the personnel determining outcome. It should be noted thst the majority of these "asphyxiated" babies, diagnosed on the basis of low Apgar scores, have no neurological sequelae.28,29

Recently, umbilical cord pH has been used to define asphyxia in terms of newborn acidemia. However, this has been questioned, and values as low as 7.10 may be associated with good outcome.20'21 Thus, umbilical artery pH values <7.10 may be more indicative of significant acidosis and asphyxia than values above this. Further, the association of low Apgar scores and acidotic cord pH values with meconium-stained amniotic fluid may reach statistical significance without having any clinical relevance. Thus, to assess the risk of abnormal outcome for term infants, one must look to true morbidity, ie, respirato' ry distress and neurological sequelae.

Figure 2. Decision tree for evaluating fetal scalp blood sampling.

Figure 2. Decision tree for evaluating fetal scalp blood sampling.

Although controversy exists regarding the significance of meconium-stained amniotic fluid, our data demonstrated that moderate or thick meconiumstained amniotic fluid marked a patient for three times the risk for adverse neonatal outcome, regardless of other risk factors. Additionally, a fetal heart rate tracing with tachycardia, prolonged bradycardia, or maternal disease increases the risk more than twofold (Table 1). Thus, just as the presence of an abnormal fetal heart rate tracing or high-risk maternal condition requires increased fetal surveillance, the presenee of thick meconium-stained amniotic fluid suggests one should reassure fetal well-being by normal fetal scalp sampling, satisfactory scalp stimulation using an atraumatic clamp, or vibroacousttc stimulation using an artificial larynx placed on the mother's abdomen over the fetal head region for 5 seconds (Figures 1 and 2). A fetal heart rate acceleration of 15 beats/minute for 15 seconds correlates with a normal fetal scalp sample.30'*2

ELECTRONIC FETAL MONITORING

Definitions

The normal baseling fetal heart rate is between 120 and 160 beats/minute (Table 2). Isolated rates of 100 to 1 19 beats/minute do not appear EO be indicative of stress, and rates may be slightly higher in the preterm fetus. Baseline abnormalities include bradycardia, tachycardia, abnormal variability, and sinusoidal patterns.

Moderate bradycardias of 80 to 100 beats/minute may be due to head compression. Severe bradycardia (<80 beats/minute) may represent fetal acidosis when prolonged >3 minutes. Fetal heart block would be the one exception.

Mild tachycardia occurs at 161 to 180 beats/minute and severe tachycardia at >180 beats/minute. Such rhythms may indicate significant fetal stress when they persist longer than 10 minutes, especially when accompanied by other abnormal patterns. Most monitors have an upper limit of 220 to 240 beats/minute and may halve the rate recorded at this level or above.

Variability refers to beat-to-beat changes; normal is 3 to 7 beats/minute, and increased variability is >7 bpm. When present, these patterns indicate fetal well-being, but are nonspecific. Absent or minimal baseline variability means a flat or nearly flat fetal heart rate, with <3 beat-to-beat changes and fewer than two cyclic changes per minute of long-term variability, ie, crossings of baseline or average fetal heart rate. Absent or minimal variability may reflect a sleep cycle, drug effects, neurologic abnormalities, or a decrease in fetal autonomie function. This decrease may interfere with the fetus' ability to adapt to the physiologic stress of labor.

A sinusoidal heart rate pattern refers to a regular oscillation of the fetal heart rate with a fixed cycle of 3 to 5 cycles per minute and an amplitude of 5 to 15 beats/minute, lasting at least 10 minutes. Classically, this pattern is associated with chronic fetal anemia, but it may follow the use of alphoprodine or other anesthetic drugs (meperidine and leutopleanol) and may not reflect fetal distress. Greater amplitudes with similar patterns are referred to as undulating and can indicate significant fetal compromise.

Only electronic fetal monitoring can be used to detect periodic fetal heart rate changes. These include accelerations, and early, variable, and late decelerations. An acceleration is an increase in fetal heart rate of at least 1 5 beats/minute for 1 5 to 20 seconds. Accelerations are thought to indicate fetal well-being whenever they occur, antepartum or intrapartum. An early deceleration is a symmetrical decrease in fetal heart rate that mirrors a contraction and is usually due to head compression. Early decelerations do not normally indicate fetal distress.

Variable decelerations are acute decreases in fetal heart rate that resemble a "U," "V, " or "W" shape and may not be related to uterine contraction. Mild varibles are generally of no consequence, but when they become severe (decrease by 60 beats/minute or measure 60 beats/minute for 60 seconds or more - rule of "60s") and are repetitive, they may herald fetal compromise.

Late decelerations are symmetric decreases in fetal heart rate that begin at or after the peak of the uterine contraction and return to baseline only after the contraction has ended. Repetitive "lates" are ominous findings and require further work-up to rule out fetal ácidos is.

Table

TABLE 2Definitions

TABLE 2

Definitions

INTERPRETATION OF ELECTRONIC FETAL MONITORING

Pioneers such as Caldeyro-Barcia,6 Hon," Paul,^ Kubli," Krebs,8 Schifínn,36 and Cibils" have studied electronic fetal monitoring over the last 30 years or so. They have made it apparent that some electronic fetal monitoring patterns are associated with fetal compromise, but the false-positive rates are high. This is because we are not sure which combinations of cardiotocogram abnormalities do not result in significant morbidity. We do not know which fetal heart rate patterns alone or in combination are not associated with a significantly increased risk for adverse neonatal outcome.

Despite the extensive work in this area, there remains considerable controversy about intrapartum electronic fetal monitoring. Despite 20 years of experience, the anticipated technologic benefit has not materialized. In addition, electronic fetal monitoring has become associated with some undesirable side effects that include inappropriate operative intervention for some patients and increased liability for physicians and hospitals, resulting in ar increase in the costs of obstetric services and malpractice insurance.38

Figure 3. Evaluating electronic fetal heart rate monitoring.

Figure 3. Evaluating electronic fetal heart rate monitoring.

This liability comes in part from the mistaken assumption, fostered in part by the legal profession, that any fetal heart rate tracing abnormality can be an indication of whatever neonatal disaster has occurred. These factors have the rising cesarean section rate. The identification of combinations of patterns that confer no increased risk would thus reassure the physician that there is no need for intervention and no breach of "standard of care."

Spontaneous accelerations have been shown to be reassuring, both antepartum and intrapartum.39'40 More recently, evoked accelerations have been shown to indicate a nonactdotic fetus,30'31 and accelerations are reassuring even in postdate pregnancies with meconium passage.41 Combinations of fetal heart rate tracing abnormalities using fetal heart rate accelerations as a discriminator may further aid in developing criteria for fetal health.

The key finding of our studies is that electronic fetal heart rate monitoring can be used to identify a small group of patients at increased risk for abnormal outcome.42 Further evaluation of these fetuses with scalp sampling could help limit cesarean section rates. The use of fetal heart rate accelerations during the last 30 minutes of labor makes it is possible to develop a low-risk profile for the great majority of tracings. Additionally, scalp pH values <7.15 further reduce the remaining group at high risk for poor outcome to only 3% of patients.

In summary, patients with no accelerations and severe variable or late deceleration, or prolonged bradycardia, tachycardia, or any combination of these fetal heart rate patterns form a high-risk group for abnormal outcome and should undergo further evaluation, such as scalp stimulation or sampling. In contrast, the fetus with fetal heart rate accelerations or mild variables, decreased variability, baseline bradycardia, or any combination of these patterns can be considered at low risk for an abnormal outcome and does not require further intervention. Infants with these reassuring fetal heart rate patterns, then, are not at increased risk for birth injury over fetuses with an absolutely perfect tracing. The attending physician using these guidelines should not be considered at fault for allowing labor to continue, regardless of the outcome.

Table

TABLE 3Electronic Fetal Monitoring

TABLE 3

Electronic Fetal Monitoring

RISK FOR ADVERSE OUTCOME

The high incidence of nonreassuring fetal heart rate patterns and poor correlation with outcome have prompted the search for fetal heart rate tracing scores and combinations of patterns as better indicators of intrapartum fetal distress. Although controversy exists regarding the advantage of electronic fetal monitoring over auscultation, our data42 demonstrated that combinations of fetal heart rate tracings (that may be difficult to auscultate) that include the absence of fetal heart rate accelerations with severe variable or late decelerations, and tachycardia mark a patient for more than two times the risk for adverse neonatal outcome (Figure 3). Additionally, a fetal heart rate tracing with these patterns and an abnormal pH increases this risk tenfold compared with patients with a reassuring fetal heart rate tracing (Table 3).

Our research eetablished that a "normal" fetal heart rate tracing, ie, with fetal heart rate accelerations, normal baseline rate, mild bradycardia (mean: 109 beats/minute), and no periodic changes other than mild variable decelerations without considering variability status, can be considered reassuring for the pregnancy at term.

MANAGEMENT OF NONREASSURING FETAL HEART RATE

If these high-risk fetal heart rate patterns, tachycardia, severe variable, or late decelerations continue, intervention is determined by the assessment of the likelihood of severe hypoxia and metabolic acidosis, and the interval needed to obtain a vaginal delivery. Persistent late decelerations, with or without tachycardia, are always nonreassuring and require action unless they resolve spontaneously or with conservative measures (oxygen, hydration, or repositioning). In this setting, a fetal electrode should be placed when possible.

The presence of spontaneous accelerations of >15 beats/minute lasting at least 15 seconds nearly always indicates normal fetal acid-base status. Fetal scalp stimulation or vibroacoustic stimulation can be used to induce accelerations, confirming a normal pH.n>u Conversely, there is approximately a 50% chance of acidosis in the fetus who does not respond to stimulation when accompanied with an abnormal tracing,30,32 In such cases, ascertainment of a fetal scalp blood pH may be used to differentiate the fetus in jeopardy. Although this technique is helpful in such cases, it is used uncommonly outside of academic centers.31 If the fetal heart rate pattern remains nonreassuring, either induced accelerations or repeat assessment of scalp blood pH is required every 20 to 30 minutes to gain reassurance. Without such assurance, the fetus should be delivered promptly by the most expeditious method.

REFERENCES

1. Barron DH. The exchange of the respiratory gsses in the placenta. Neonatal Stud. 1952; 1:3- 1 5.

2. Apgar V. A proposal far a new method of evaluation of the newborn infant. Curr Res Anesth Analg. 1953:32:260-268.

3. James LS, Weisbrot IM, Prince CE, et al. The acid-base status of human Intents in relation to birth asphyxia and the onset of feipiration. J Pediatr. 1958:52:379-384.

4. Saling E. Neuea vorgehen zui Untersuchung des klndes unter der gebnit. Arch Gynatol. 1961; 197:108-116.

5. Hon EH. Quillfgan EJ, The clarification of fetal heart rate, 11: a revised working classification. Conn Med. 1967:31:779-736.

6. Caldevro-Barcia R, Casacuberta C, Bustos R, et al. Correlation of lntrapartum changes in fetal heart rate with fetal blood oxygen and acid-base balance. In: Adamsons K, cd. Diagnosis and Treatment of Fetal Disorders. New York, NY: Springer-Verlag; 1968:205-224.

7. Miller PC, Read JA. Intrapamim assessment of the postdates fetus. Am J ObsteGynecol 1981:141:516-521.

8. Krebs HB, Peten RE, Dunn LJ, et al. lntrapartum fetal heart rate monitoring. III: association of mcconium with abnormal fetal heart rate pattern). Am J Obscet Gynecol. 1980:137:936-940.

9. Cole JW, Portman RJ, Lim Y, et al. Urinary beta-2-microglobulln In full-term newborns: evidence for proximal tubular dysfunction In infants with meeonium-stained amnlotic fluid. Pediatrics. 1985:76:956-962.

10. Starks GC. Correlation of meeonium-stained amniotic fluid, early intrapartum fetal pH and Apgar scores as predictors of perinatal outcome. Obstet Gynecol. 1980:56:604-608.

11. Düxhoom MJ, Visser GHA, Fidler FJ, et al. Apgtr scores, meconium and acidemia at birth in relation to neonatal neurological morbidity in term infants. Am J Obstet Gynecol. 1986:93:217-221.

12. Dooley SL, Pesavento DJ, DeppR, et al. Meconium below the vocal cords at delivery: correlation with intraparnim events. Am J Obstet Gynecol. 1985:153:767-771.

13. Mela PJ, Hobel CJ, Uteda JR. Late mecociium passage in labor - a sign of fetal disitesi! Obstet Gynecol. 1982:59:331 -336.

14. Mitchell J, Schulman H, Fleucher A. et al. Meconlutn aspiration and retai acidosis. Obstet Gynecol 1985:65:352-356.

15. Gregory GA. Goading CA. Meconium aspiration in infants - a prospective study. J Pediatr. 1974:85:848-852.

16. Abramovici H, Brandes JM, Fuchi K, Timor-Tritsch I. Meconium durine delivery: a sign of compensated fetal distress. Am J Obstet Gynecol 1974;116:251-255.

17. Fenion AN. Steer CM. Fetal distress. Am J Obstet Gynecol 1962;83:354-358.

18. Hobel CJ. Intrapartum clinical assessment of fetal distress. Am I Obstet Gynecol. 1971:110:336-340.

19. Miller FC, Sacks DA, Yeh SY, et al. Significance of meeonium during labor Am J Obstet Gynecol. l975;122:573-577.

20. Yeomans ER, GiUtrap LC, Leveno KJ, Burrli JS . Meconium in the amniotic fluid and fetal acid-base status. Obstet Gynecol. 1989:73:175-179 .

21. Mas PJ, Hall M, Marshall JR, Hobel CJ, Meconium passage: anew classification for risk assessment during labor. Am J Obstet Gynecoi. 1978;! 3 1:509-5 13.

22. Trimmet KJ, Gllstrap LC. "Meconiumcrit' and birth asphyxia. Am J Obstet Gynecol. 1991;165:1010-1014.

23. Baker PN, Kilby DM, Murray H. An asseiment of the use of meconium atone aa an indication for fetal blood sampling. Obstet Gynecol. 1992;80:792-796.

24. Altshuler G, Hyde S. Meconium -Induced vasocontraction: a potential cause oí cerebral and other fetal hypoperfislon and of poor pregnancy outcome. J Child Neurol. 1989:4:137-142.

25. Altshuler G, Ariiawa M, Molinar-Nadaidy G. Meconlum-induced umbilical vascular necrosis and ulceration: a potential link between the placenta and poor pregnancy outcome. Obstet Gynecol. 1992; 79: 760-766.

26. Benlrechke K, Kaufmann P, eds. Pathology of the Human Piacente, 2nd ed. New York, NY: Springer-Verlag; 1990.

27. Berkus MD. Langer O. Samueloff A. Xenakls EMJ. Field NT, Rldgway LE. Meconium-atained amniotic fluid: increased risk for adverse neonatal outcome. Obstet Gynecol. 1994:84:115-120.

28. Weitzner JA, Stnusntr HT. Rawlins RC. et al. Objective assessment of rnccanlum content of amniotic fluid. Obstet Gynecol. 1990:76:4143-4144 .

29. Paul RH, Petrie RH. Fetal Imeruwc Care. Val 2. Case Management. North Haven, Conn: William Mack Co; 1979.

30. Clark SL. Grivovsky ML, Miller FC. Fetal heart rate response to scalp blood sampling. Am J Obstet Gynecol. 1982:144:706-708.

31 . Clark SL, Paul RH. lntrapartum telai surveillance: the role of fetal scalp blood sampling-Am J Obstet Gynecol. 1985:155:717-720.

32. Smith CV, Nguyen HN. Rielan JP, Paul RH. Intrapartum aaseument of fetal well-being: a comparison of fetal acoustic stimulation with acid -base determination. Am J Obstet Gynecol. 1986:155:726-728.

33. Hon EH. Detection of fetal distress. In: Wood C. ed. Fifth World Congres of Gynecolofy and Obaema. Sydney, Australia: Butterworths. 1967:58-84.

34. Paul RH. Hon EF. Clinical monitoring, V: effect on perinatal outcome. AmJ Obstet Gynecol. 1974:118:529-534.

35. Kubli FW, Hon EH, Khaiin AF. Takemura H. Observations on bean tate and pH In the human fetus during labor. Am J Obstet Gynecoi. 1969;104: 190-1205.

36. Schlftrln BS, Dame L. Fetal bean rate patterns: prediction of Apgar score, JAMA. 1972:219:1322.1325.

37. Cibili LA. Clinical significance of fetal heart rate patterns during labor, I: baseline patterns. Am J Obstet Gynecol. 1976; 12 5:290-305.

38. Sandmire HE Whither electronic fetal monitoring? Obstet Gynecol. 1990:76:11301134.

39. Tejani N, Mann L, Bharthavathsaian A, Weist RR. Correlation of fetal heart rateuterine contraction patterns and fetal scalp blood pH. Obstet Gynecol. 1975:46:392396.

40. Rochad F, Schlfrln BS, Goupil F, et al. Nonstrcoecd fetal heart rare monitoring in the anteparrum period. Am J Obstet Gynecol. 1976:126:699-707.

41. Shaw K. Clark SL. Reliability of Intrapartum fetal heart rate monitoring in the postterm fetus with meconium passage. Obstet General. 1988:72:886-889.

42. Berkus M, Samueloff A. Langer O. Xenakii E. Rldgway L. Intrapartum electronic fetal monitoring: how abnormal Ii abnormal? Presented at the 39th Annual Meeting of the Society for Gynecologic Investigation: San Antonio, Texas; March 18-21, 1992.

TABLE 1

Risk for Adverse Outcome

TABLE 2

Definitions

TABLE 3

Electronic Fetal Monitoring

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