MaternalFetal Medicine

Electronic Fetal Heart Rate Monitoring Risks, Benefits, Future, and Strategies to Avoid Pitfalls
a report by

Thomas J Garite, MD
Professor Emeritus, Obstetrics and Gynecology, University of California Irvine

Methods for the evaluation of the fetus in labor have a long history. What seems surprising is that the purpose and goals of this evaluation are often unclear, and what we can accomplish with the available technology is often overestimated. Therefore, in this article we will review the development of electronic fetal heart rate monitoring (EFM), the purpose of this modality, its benefits, limitations, pitfalls, and downsides, and what we need to do in the future to improve intra-partum (IP) fetal evaluation. Purpose There are a number of real and imagined purposes of EFM. The prevention of IP fetal death is the most easily defined and realistic goal. Prior to EFM, IP deaths occurred in about three per 1,000 labors, or one per month in a typically busy obstetric unit.1 The elimination of IP fetal death in labor has essentially become a near reality. This event is now extremely rare and usually occurs either because EFM is not properly used or the death is so sudden and unpredictable that there was not time to respond (e.g. ruptured vasa previa and rapid fetal exsanguination). The elimination of long-term neurological damage to the baby, particularly cerebral palsy (CP), is one of the most elusive and misunderstood goals of EFM. Clearly, one of the consequences of asphyxia in labor is damage to fetal organs, and the central nervous system is especially vulnerable. Therefore, an ambitious and perhaps unrealistic goal of EFM has always been to eliminate CP and other neurological injuries. To prove that EFM contributes to the reduction of such injuries has become particularly difficult because there are so many other causes of these problems such as toxins (e.g. methyl mercury), infections (e.g. cytomegalovirus [CMV]), genetic diseases, drug abuse, etc., and also because asphyxic injuries may occur prior to labor, and the timing of the injury is often difficult or impossible to establish. At most, only about 25% of neurological injuries occur during labor.2 Since these events are rare, to prove that a reduction by half of the one-quarter of cases actually caused by asphyxia during labor of the four per 1,000 rate

of CP means that one would have to prove that one in 1,000 would be reduced to 0.5 in 1,000. This is a nearly impossible task for randomized trials because of the huge number of patients that would be required to prove this, and because of the need for long-term follow-up of so many babies. Other goals that are perhaps more realistic but as yet not proved or evaluated are a reduction in short-term neonatal injuries, especially meconium aspiration, and a reduction in complications of prematurity. Both of these complications are known to be exacerbated by IP asphyxia. To approach these issues more specifically and more realistically would seem to be a logical and important way to improve our understanding of EFM. Except in exceedingly rare cases, the causes of fetal death in labor are asphyxia (hypoxia leading to metabolic acidosis and the subsequent series of events leading to tissue damage and death), trauma, or infection. Generally speaking, trauma is a consequence of the birth process and cannot be prevented by the monitoring of labor. Bacterial infections in labor certainly cause fetal death, but unless the infection is so severe that it is at a stage where the fetus is hypoxic and acidotic due to shock, the FHR manifestations of sepsis are so non-specific that EFM cannot realistically be expected to have an effect on outcome. The detection of impending asphyxia is a realistic and specific goal of EFM. Fetal hypoxia and acidosis cannot exist without specific changes in the FHR. A normal FHR tracing virtually proves that the fetus is not hypoxic and/or acidotic. Thus, when evaluating the FHR tracing in labor, we should be more careful to be more specific about what we are trying to assess and accomplish. Statements such as your baby is fine imply that we can tell more about the fetus than we actually can. More specific statements such as the baby is getting enough oxygen allow us to focus more specifically on what we should and can accomplish with EFM. Some brief statements can be made to allow us to understand the physiological basis of FHR monitoring. To begin with, let us understand that there is an orderly cascade of the development of fetal asphyxia (see Figure 1). First, the fetus suffers from a deficit in the amount of oxygen delivered. This may occur because the fetal lung (its placenta) is not getting enough oxygen, as found with hypotension or excessive contractions; not exchanging oxygen within itself, as with prolonged pregnancy or actual placental disease; or sometimes (rarely) because the fetus cannot adequately pick up oxygen from the plalcenta, as with severe fetal anemia. Additionally, the fetus may not get enough oxygen because its windpipe (the umbilical cord) is obstructed, as with umbilical cord compression or stretch. If the oxygen deficit is severe enough and lasts for long enough, the fetus will have to metabolize anaerobically, and will begin to develop a

Thomas J Garite, MD, is the recently retired Edward H Quilligan Professor of Obstetrics and Gynecology at the University of California Irvine, having served 18 years as the Departments Chairman. He is Editor In Chief of the American Journal of Obstetricians and Gynecology, President of the Society of Maternal Fetal Medicine Foundation (SMFM), and Director of Research and Education for Obstetrix, Pediatrix Medical Group. He has received many awards, including the Career Achievement Award from the Society of MaternalFetal Medicine (SMFM) and the National Teaching Award from the Association of Professors of Obstetrics and Gynecology (APGO)/Council on Residency Education in Obstetrics and Gynecology. E: Thomas_Garite@pediatrix.com

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Electronic Fetal Heart Rate MonitoringRisks, Benefits, Future, and Strategies to Avoid Pitfalls

metabolic acidosis. If the metabolic acidosis is severe enough and lasts for long enough, tissue damage will occur and the fetus will either become damaged or die if an intervention to reverse the process by delivery and resuscitation of the baby does not occur. Fortunately, the FHR of the baby can accurately depict the malfunctions that can lead to fetal hypoxia. In a laboring mother, the fetus will always experience decelerations that warn of the presence of hypoxia. Late decelerations tell us that the placenta is not providing enough oxygen, and variable decelerations can indicate hypoxia due to umbilical vascular blockage. However, to diverge, although the primary reflex for umbilical cord patterns, i.e. variable decelerations, is a baroreceptor reflex caused by the blood pressure changes that occur with umbilical cord obstruction, as these decelerations become deeper and last for longer hypoxia becomes more likely. Sudden and profound hypoxia (due to either placental or cord problems) can also lead to prolonged deceleration and bradycardia. Other changes in the FHR such as tachycardia and loss of variability and loss of accelerations are not due to hypoxia per se, but to the consequences of hypoxia and developing acidosis. In a laboring patient with developing hypoxia and acidosis, variable, late, or prolonged decelerations will come first, and as the hypoxia becomes more severe tachycardia and/or a loss of accelerations and loss of variability develop as the baby begins to become acidotic. Thus, the FHR of the fetus will tell us when the baby is hypoxic and acidotic, and at least where the problem is. Unfortunately, the problem with EFM is not that the hypoxic baby will not be detected, but that many other things will affect the FHR besides hypoxia. Fetal head compression during labor can cause early decelerations, easily confused with late decelerations, and can also cause changes that mimic variable decelerations. Drugs or medications can alter the FHR. Fetal diseases or anomalies can lead to confusing FHR patterns. Previous neurological injury, not amenable to delivery and resuscitation, can cause profound FHR changes. Temperature alterations, both fever and hypothermia, will change the FHR. Thus, the major problem of EFM is its lack of specificity. This means that while the FHR will always be abnormal in the presence of significant hypoxia, when the FHR is abnormal this is more often due to causes other than hypoxia. Put another way, a baby who is born hypoxic and acidotic will always have had an abnormal or non-reassuring FHR, but most babies with abnormal or non-reassuring FHR patterns will be born well oxygenated and will be vigorous at birth.3 Another major problem with EFM is that it is based on pattern recognition, and care-givers and even experts cannot agree on abnormal patterns. Care-givers given the same strip weeks apart will often differ in interpretation from their original description. Even the computer interpretation of EFM has eluded us. These are the bases of the many pitfalls of IP EFM. These pitfalls include an over-reaction to FHR patterns that are not associated with hypoxia. This leads to unnecessary interventions that increase anxiety for patients, such as when the nurse uses oxygen on the mother or performs other interventions, or unnecessary operative delivery takes place. Expectations that EFM will lead to a perfect outcome lead to the blame and litigation that ensues when a baby is not perfectly normal.

Figure 1: Model for Declining Fetal Respiratory Status and the Development of Hypoxia, Acidosis, and Death

Normal oxygenation

Hypoxia

Acidosis

Tissue damage/death

Table 1: Common Problems with Electronic Fetal Heart Rate Monitoring

Failure to adequately evaluate on admission Inadequate tracing Failure to communicate severity of pattern Failure to recognize severity of pattern Failure to use common nomenclature Failure of doctor to attend when nurse expresses concern Delayed response time Issues with oxytocin administration and hyperstimulation

A review of extensive experience with lawsuits alleging substandard care with respect to EFM has led to a list of key problem areas (see Table 1). The following suggestions are made to assist care-givers with improving care and outcome, and to decrease litigation related to problems with EFM. First, physicians, midwives, and nurses require ongoing education. This can be accomplished in a number of ways, but recently both individual hospitals and large hospital consortia have developed requirements for staff stating that an annual course be taken and documented. One such Internet-based educational program can be found at www.healthstream.com/hlc/hca-mdu Second, it is advised that all triage patients who are beyond 24 weeks of gestation receive a monitoring strip prior to discharge, and that all non-reassuring or questionable strips be reviewed by a physician. Third, there must be a hospital policy put in place to determine which patients require internal FHR and/or contraction monitoring. Not all patients require internal monitoring, and this is true even of those with non-reassuring strips, but when an accurate FHR trace cannot be obtainedespecially when there is any question regarding the reassuring status of the fetusan internal electrode should be placed. Fourth, a nurse should initial the FHR strip every 15 minutes. Many hospital policies require that nurses perform extensive charting concerning every detail of the FHR in labor. Such policies are a waste of

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time and remove the nurse from the patient. A simple policy, called charting by exception, would create written definitions of what constitutes a reassuring tracing and ask the nurse to initial the tracing every 15 minutes as long as the FHR fits these criteria. When the FHR does not meet these criteria, the physician should be notified and the nurse should perform the appropriate interventions and make a chart entry describing what is seen and what was done. Fifth, a physician is required to review all non-reassuring and questionable patterns. This may be done in person or electronically, but there should never be any argument; when the nurse has a concern, the physician should review the strip. Sixth, a hospital should be able to achieve a 30-minute response time to perform a Cesarean section whenever an FHR pattern indicates that such an urgent intervention is required. Policies to ensure nursing, operating room, anesthesia, and obstetric physician staff are available to accomplish this should be created. Many hospitals are now performing unexpected drills at random times to see whether this can be consistently performed. The seventh recommendation concerns oxytocin problems, which are among the most consistently alleged issues of substandard care in the event of a bad outcome. Clark4 has made the following recommendations to avoid this issue: there should be checklists for oxytocin useone for induction and one for augmentation; a history and physical should be undertaken, and a physician must order oxytocin. The physicians note should include that the pelvis is clinically adequate, and indicate oxytocin; an estimated fetal weight should be on the chart from within the past week; the physician should be readily or immediately available as defined locally by hospital protocol; one-on-one nursing should be provided whenever possible; EFM criteria for continuing oxytocin should be established. Suggestions for such criteria include no late decelerations within the last 30 minutes, and no variable decelerations to <60bpm for >60 seconds within the last 30 minutes. A physicians note should be required to continue oxytocin for any exception to the above; contraction criteria should be defined: adequate recording of contractions should be documented or monitored with intrauterine-pressure catheter (IUPC), uterine contractions (UCs) should not exceed five to 10 minutes, and no two UCs should last >120 seconds in a 30-minute period. If IUPC is used, Montevideo Units should be <300 and resting tone <25; and a protocol should be established for the oxytocin dosing regimen. When an exception to this protocol is made, a written order and note explaining why should be required.

Where do we need to go now with EFM? Clearly, any technology with a high sensitivity and poor specificity, such as EFM, should have a back-up method. When the FHR is reassuring, care-givers are well trained, and the monitor is carefully watched, mistakes that can result in hypoxic damage to the baby will rarely be made, since there will never be an oxygen deficit with a reassuring FHR pattern. There are specific circumstances where FHR can accurately be relied upon to identify hypoxia and acidotic fetuses. These include persistent late decelerations with absent variability, persistent severe variable decelerations with tachycardia and absent variability, and persistent bradycardia with absent variability. However, most non-reassuring FHR patterns do not meet these criteria, and in these situations the fetus is more often not hypoxic. How can we be sure and do we want to take a chance on the babys outcome when we cannot be sure? The answer is of course no, and that is why there are so many unnecessary but appropriate operative interventions. What we desperately need is a back-up method that has excellent specificity for hypoxia and/or acidosis. Fetal scalp pH monitoring was the original method used, and is still in widespread use in parts of Europe, but it is infrequently used in the US because it is cumbersome and the volume of blood obtained does not allow the determination of partial pressure of carbon dioxide (pCO2) and ruling out a respiratory acidosis that is not significant. Continuous pH monitoring using a glass electrode was attempted but never perfected. There was great hope that fetal pulse oximetry would be the answer to this problem, but, for various reasons, including the fact that the technology was rolled out before it was perfected, its popularity and utilization (which had a brief flurry of success) waned and the product is no longer produced in the US. This technology is theoretically ideal, and will perhaps re-emerge at some point in the future. Currently, the only technology available that shows great promise to back up EFM is the STAN technology, which is a computer-based analysis of the EKG waveform and is apparently a more specific way of defining fetal hypoxia. There are two very good prospective randomized trials in Europe that suggest that this technology not only decreases the need for unnecessary operative intervention, but may even decrease the likelihood of delivering a baby with severe metabolic acidosis.5,6 Trials in the US are at the planning stage, and the machines are currently being used in several pilot hospitals. Obstetrics is not unique in its quest for a technology that improves patient outcome. The labor and delivery unit is a true intensive care area, and dangerous and unexpected things can and do happen. The technology of EFM is imperfect in many ways, but it is what we have. Therefore, we are obliged to understand it, to continually improve our expertise in its use, and to apply it appropriately and carefully.

1. 2.

3.

Freeman RK, Garite TJ, Nageotte MP, Fetal Heart Rate Monitoring, 3rd Edition, Philadelphia: Lippincott, Williams & Wilkins, 2003. Joint publication of the American College of Obstetricians and Gynecologists and the American Academy of Pediatrics, Neonatal Encephalopath and Cerebral Palsy, 2003. Shifrin BS, Dame L, Fetal heart rate pattern. Prediction of Apgar

4. 5.

score, JAMA, 1972;219:1322. Clark SL, Oxytocin, new perspectives on an old drug, Am J Obstet Gynecol, 2008; in press. Westgate J, Harris M, Curnow JSH, Greene KR, Plymouth randomised trail of cardiotocogram only versus ST waveform plus cardiotocogram for intrapartum monitoring, 2,400 cases, Am J

6.

Obstet Gynecol, 1993;169:115160. Amer-Whlin I, Hellsten C, Noren H, et al., Cardiotography only versus cardiotocography plus ST analysis of fetal electrocardiogram for intrapartum fetal monitoring: a Swedish randomised controlled trial, Lancet, 2001;358:5348.

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