- Email: [email protected]
The Current Crisis in Obstetrics
COMMENTARY
The Current Crisis in Obstetrics James A. Low, MD Department of Obstetrics and Gynaecology, Queen's University, Kingston ON
Abstract
une conclusion, au sujet du moment ou sont survenues les lesions cerebrales, en fonction de la preponderance des probabilites.
Of the issues leading to legal actions in obstetrics, the most important are events occurring before delivery that are deemed to account for the birth of a physically or mentally challenged child.
Bien qu'il so it d'une certaine utilite, la determination du risque clinique au moyen de la surveillance de la frequence cardiaque fcetale (FCF) peut generer des resultats faux positifs en matiere de prediction de I'asphyxie intra-uterine. Le probleme, dans Ie cas de la surveillance de la FCF, c'est I'absence d'un algorithme detaille pour I'interpretation des traces de FCF comptant des recommandations appropriees en matiere de prise en charge. Jusqu'a ce qu'un tel algorithme soit elabore, on ne peut s'attendre a ce que les intervenants en sante reagissent de fayon uniforme aux traces de frequence cardiaque fcetale.
In determining causation in the clinical setting, the diagnosis of fetal asphyxia can be made using blood gas and acid-base assessment. However, there are many subsidiary questions that in most cases cannot be answered, including when the asphyxia began, the severity and nature of the asphyxia during the exposure, the quality of the cardiovascular compensation, and when the brain damage occurred. When scientific proof is not available, the dilemma for the court is the requirement to reach a conclusion about the timing of brain damage on the balance of probabilities. Although it is of value, clinical risk scoring using fetal heart rate (FHR) monitoring may result in false positive predictions of fetal asphyxia. The problem in FHR monitoring is the lack of a detailed algorithm for the interpretation of FHR patterns with appropriate recommendations for management. Until such an algorithm is developed, health care workers cannot be expected to respond·to fetal heart rate patterns consistently. Responsibility for the crisis in obstetrics must rest with the members of the health care disciplines who provide expert testimony. Progress made in research encourages us to assume that more is known about the causes of brain damage in the clinical setting than in fact is known. Similarly, health care professionals, parents, and lawyers often assume current methods of prediction and diagnosis to be more effective than they actually are.
Resume Les evenements qui surviennent avant I'accouchement et qui sont tenus pour responsables de la naissance d'un enfant presentant une deficience physique ou mentale constituent les plus importants motifs de poursuites judiciaires dans Ie domaine de I'obstetrique. Lorsque vient Ie temps de determiner les causes d'un tel evenement en milieu clinique, il est possible de poser un diagnostic d'asphyxie intra-uterine au moyen d'une evaluation en fonction de la gazometrie et de I'acidite. Toutefois, il subsiste de nombreuses questions incidentes qui, dans la plupart des cas, ne peuvent etre elucidees, y compris la determination du moment a partir duquel I'asphyxie a debute, la gravite et la nature de I'asphyxie au cours de I'exposition, la qualite de la compensation cardiovasculaire, ainsi que la determination du moment ou sont survenues les lesions cerebrales. En I'absence de preuves scientifiques, les tribunaux sont confrontes au fait de devoir tirer Key Words: Fetal asphyxia, brain damage, medical legal Competing Interests: None declared. Received on March 21 , 2005 Accepted on July 21 , 2005
La responsabilite, quant a la crise que connait I'obstetrique, doit etre assumee par les membres des disciplines de la sante qui fournissent des temoignages d'expert. Les progres realises dans Ie domaine de la recherche nous poussent a presumer que les connaissances au sujet des causes des lesions cerebrales sont superieures a ce qu'eUes sont en realite. De fayon similaire, les profession nels de la sante, les parents et les avocats presument souvent que les methodes actuelles de prediction et de diagnostic sont plus efficaces qu'elles ne Ie sont vraiment.
J Obstet Gynaecol Can 2005;27(11):1031-1037
INTRODUCTION
I
n 2004, the Canadian Medical Protective Association fees in Ontario for physicians practising obstetrics ($86244) were 10 times the average of fees for all health care disciplines ($8783). These fees reflect the number of new fJles opened, threats of medico-legal difficulty, legal actions commenced, legal actions proceeding to trial, and judgements for the plaintiff. Does this imply that physicians providing obstetric care are 10 times less competent than physicians in other disciplines? That they are10 times more likely to make mistakes? That they care 10 times less for patient welfare? If we assume that these statements are not true, then what is the problem? By far the most important reasons for such medical-legal actions are events occurring before delivery that are considered to account for a child's being physically and possibly mentally challenged. 1 Two issues arising from these legal actions are causation and standard of care. The cause receiving most attention is fetal asphyxia. The standard of care is usually assessed by the paradigm of fetal monitoring before and during labour, which is designed to predict and establish a diagnosis of fetal asphyxia.
NOVEMBER JOGe NOVEMBRE 2005.
1031
COMMENTARY
The objective of this review is to examine our current understanding of the relationship between fetal asphyxia and brain damage, and the characteristics of the current paradigm for the prediction, diagnosis, and management of fetal asphyxia. FETAL ASPHYXIA AS A CAUSE OF BRAIN DAMAGE
Clarifying the significance of fetal asphyxia as a cause of brain damage began in the mid-20th century when the systematic examination of the effect of asphyxia and ischemia on the fetus began in the research laboratory. These studies have provided the foundation for our understanding of the relationship between fetal asphyxia and brain damage. The initial studies demonstrated that total fetal asphyxia lasting more than 12 minutes 2- 5 and partial fetal asphyxia lasting more than 60 minutes 6- 8 may cause brain damage, with severe metabolic acidosis and hypotension found consistently before brain damage occurred. The outcome of a uniform single episode of fetal asphyxia has been strikingly variable, ranging from no brain damage in many fetuses to brain damage in some and to fetal death in a few. This variability of outcome is due in large part to the fetus's' compensatory cardiovascular response to asphyxia. There is a redistribution of cardiac output with increased blood flow to the brain, heart, and adrenals: 9- 12 the balance between the quality of the fetal' cardiovascular response and the degree and duration of fetal asphyxia may determine whether or not the asphyxia leads to brain damage. However, as studies have continued, this relationship has become more complicated. The immature fetus differs from the mature fetus. Total cord occlusion studies indicate that the immature fetus will survive a longer period of asphyxia. Following a more prolonged episode of asphyxia, this capacity to survive exposes the immature fetus to sudden decompensation with profound hypotension and hypoperfusion. 13- 15 Fetal asphyxia may be a recurrent event, and repeated episodes may have a cumulative effect with brain damage even if individual episodes would not cause brain damage. 16- 18 Intrauterine infection is a confounding factor. Coliform endotoxemia, with release of circulating proinflammatory cytokines, will compromise fetal cardiovascular function. The mechanism of fetal cardiovascular compensation is not effective against the hypoxemia associated with endotoxemia or a concurrent exposure to fetal asphyxia. 19- 22 Brain damage that follows fetal asphyxia with concurrent fetal infection may develop because of both increased sensitivity to hypoxemia-ischemia and the direct effect of cytokines in the brain.
1032 • NOVEMBER}OGC NOVEMBRE 2005
Recent laboratory studies of placental insufficiency suggest an entirely different mechanism of brain damage. Placental insufficiency induced for 20 to 30 days in sheep, causing fetal hypoxemia without metabolic acidosis, resulted in brain damage prominent in the cerebral white matter. 23,24 As these studies have continued, the complexity of the relationship between fetal asphyxia and brain damage has become apparent. FETAL ASPHYXIA AS A CAUSE OF BRAIN DAMAGE IN THE CLINICAL SETTING
The introduction of microelectrode blood gas systems permitted clinical studies that could evaluate fetal asphyxia at the time of delivery. Intrapartum fetal asphyxia must be progressive, leading to a metabolic acidosis, to be ofpathological significance. The threshold of a metabolic acidosis at delivery beyond which cerebral dysfunction may occur has been determined to be an umbilical artery base deficit greater than 12 mmol/L.25 Thus a blood gas and acid-base assessment at delivery that shows a significant metabolic acidosis confirms that fetal asphyxia has occurred. Because most methods used in the animal laboratory to assess asphyxia are not available in the clinical setting, the clinical classification of asphyxia as mild, moderate, or severe is based on the presence of metabolic acidosis (to confirm the occurrence of asphyxia) with measures of neonatal encephalopathy and other organ system complications (to express the severity of the asphyxia).26 This classification is of prognostic value, with significant newborn morbidity and brain damage occurring in some newborns with either moderate or severe fetal asphyxia. Although an umbilical cord blood gas and acid-base assessment at delivery can confirm that asphyxia has occurred, the following questions are relevant but may not have answers.
1. When did fetal asphyxia begin? A growing body of indirect and direct evidence points to the importance of antepartum fetal asphyxia as a cause of brain damage and deficits in surviving children. Although the prevalence of intrapartum fetal asphyxia as determined at delivery has been established, the duration and nature (i.e., continuous or intermittent) of the asphyxia in most cases is not known. Since the duration of the asphyxia cannot be determined, it is not known how often the asphyxia identified at delivery may have begun before the onset of labour. Since the natilre of the asphyxia cannot be determined, it is not known how often the asphyxia identified at delivery represents the last in a series of episodes of asphyxia that may have begun before the onset of labour. When asphyxia is limited to the intrapartum period, the time when the asphyxia began and the nature of the asphyxia can rarely be determined.
The Current Crisis in Obstetrics
2. What was the severity and nature of the asphyxia? Because the blood gas and acid-base status of the fetus cannot be measured continuously during labour, the severity and nature of the asphyxial exposure is rarely known. Asphyxia during labour is often perceived to be either acute (almost total) asphyxia or partial asphyxia on the basis of the initial research models that contributed to current understanding of the relationship between fetal asphyxia and brain damage. These and subsequent models were achieved by careful control of induced maternal hypoxemia, reduced utero placental blood flow, umbilical cord blood flow, or carotid artery blood flow, and such circumstances are unlikely to be duplicated in the clinical setting. This suggests that asphyxia occurs like a switch with off, mild, moderate, and severe settings, but the clinical setting is more likely to simulate a dimmer switch. 3. What was the quality of the fetal cardiovascular compensation? Without continuous measures of fetal blood pressure and organ blood flow throughout labour, the quality of the fetal cardiovascular compensation in response to fetal asphyxia is not known. Lacking this information, and understanding the complexity of the relationship between fetal asphyxia and brain damage, any speculation about the sequence of events prior to delivery will be fundamentally imprecise. 4. When did the brain damage occur? Accurately determining when brain damage occurred is impossible in the absence of information about when the asphyxia began, the nature and severity of the asphyxial episode, and the quality of the fetal cardiovascular compensation. Indirect' measures such as clinical sentinel events, abnormal FHR patterns, and ultrasound, computerized tomography (C1) scans, and magnetic resonance imaging (MRI) studies provide indirect markers in some cases. However, these observations do not provide specific insight into when the brain damage has occurred. An umbilical cord blood gas and acid-base assessment at delivery will confirm that an asphyxial exposure has occurred, and the asphyxial exposure can be classified as mild, moderate, or severe on the basis of the neonatal course. However, it is rare that an obstetric expert can give an accurate opinion about the sequence of events before delivery and specifically when the brain damage has occurred. In the case of a legal action following delivery of a brain damaged baby, the dilemma for the court is the requirement to reach a conclusion about the timing of brain damage due to fetal asphyxia on the balance of probabilities when scientific proof is not available.
STANDARD OF CARE FOR THE PREDICTION AND DIAGNOSIS OF FETAL ASPHYXIA
The diagnosis of fetal asphyxia can be confirmed by means of periodic fetal scalp blood sampling during labour or cord blood sampling at delivery for a blood gas and acid-base assessment. To define a standard of care, we need criteria to identify the fetus at enough risk for fetal asphyxia during labour to justify an intervention for fetal blood sampling for a fetal blood gas and acid-base assessment. A combination of clinical risk scoring and FHR surveillance has been widely used to identify the fetus at risk of asphyxia; however, the shortcomings of each element have become evident with increasing clinical experience. Clinical Risk Scoring The limitations of clinical risk scoring have been demonstrated in several studies. In our experience, 23% to 40% of fetal asphyxia occurred in pregnancies with no clinical risk factors. 27- 28 The term "low risk" based on clinical markers cannot be applied to the risk of fetal asphyxia during labour.
In those cases in which clinical risk factors were present, a wide range of clinical complications determined risk, and no single risk factor demonstrated a strong association with intrapartum fetal asphyxia. The positive predictive value for both antepartum and intrapartum clinical risk factors for intrapartum fetal asphyxia was 3%.27 Thus, clinical risk scoring has a very high rate of false positive prediction of intrapartum fetal asphyxia. Electronic Fetal Heart Rate Monitoring A 1958 publication by Edward Hon 29 created an expectation that electronic FHR monitoring (EFM) would be useful in the prediction of intrapartum fetal asphyxia. Observations subsequently supported the contention that EFM could be a useful screening test for the prediction of intrapartum fetal asphyxia. Our clinical experience paralleled that of other investigators in this field with anecdotal examples of an association between abnormal FHR patterns and fetal asphyxia with a range of outcomes. On the basis of such experience, the use ofEFM expanded rapidly in the 1970s.
There are two requirements for a screening test. First, the clinical problem must justify intervention. Intrapartum fetal asphyxia is important and in selected circumstances justifies intervention. Second, the benefits of the test must outweigh the harm. We recognized in the late 1970s that this had not been determined. Well-designed, randomized controlled trials are the current standard for providing a measure of the true risks and benefits of a medical intervention. There have been no randomized clinical trials to compare "no fetal heart rate monitoring" with "intermittent fetal heart rate auscultation." Nine
NOVEMBER]OGC NOVEMBRE 2005.
1033
COMMENTARY
randomized clinical trials, three with electronic fetal monitoring alone and six with electronic fetal monitoring and scalp blood sampling, have been analyzed in the Cochrane Pregnancy and Childbirth Database.30,31 The randomized clinical trials comparing intermittent auscultation and continuous EFM have not provided consistent evidence that EFM was associated with a decrease in fetal and newborn morbidity. The randomized clinical trials have made an important contribution, confirming the occurrence of false positive interpretation of EFM, with consequent unnecessary interventions. These studies have demonstrated that EFM has been associated with an increased incidence of Caesarean section for fetal distress and dystocia, operative delivery, and general anaesthesia compared with intermittent auscultation. Faced with the available evidence, national organizations began to prepare consensus papers on the subject of fetal surveillance during labour. Clinical guidelines have been recently published by the Society of Obstetricians and Gynaecologists of Canada (SOGq, 32 the American College of Obstetricians and Gynecologists (ACOG),33 and the Royal College of Obstetricians and Gynaecologists (RCOG).34 These guidelines, prepared by recognized experts in the field, reflected the best evidence available at the time of publication. What is missing from all the current guidelines is a specific algorithm for the interpretation of FHR patterns. The SOGC and the ACOG guidelines classify FHR patterns as reassuring and non-reassuring. Detailed criteria and duration are not noted. The RCOG guidelines have defined EFM traces as normal, suspicious, and pathological. No guidelines have provided information about the sensitivity, specificity, and predictive value of the patterns as defined. This issue was addressed by a National Institutes of Health (NIH) research-planning workshop in 1997. 35 Although all members of the workshop agreed that EFM was of value, there was no consensus regarding strict guidelines for clinical management using FHR patterns. The position expressed was that many fetuses have FHR tracings that are neither totally normal nor so severely abnormal that the fetus is at risk of morbidity or mortality. The workshop concluded that developing evidence-based algorithms for management will require further research. Recently, this view has been expressed again. 36 Until such specific algorithms are developed, health care workers responsible for the care of obstetric patients cannot be expected to respond to abnormal FHR patterns consistently.
1034 • NOVEMBER]OGC NOVEMBRE 2005
Clinical In terpre.ta tion of the FHR Record The following issues remain to be resolved for the interpretation of a FHR record.
1. Classification of FHR variables Many definitions of the individual FHR variables (baseline FHR, bal'eline FHR variability, accelerations and decelerations) have been provided. However, differences in the criteria for classification remain, particularly for decelerations. While such a consensus is being developed, criteria should always be clearly defined and consistently used. 2. Inter-observer reliability Although progress is being made in the computer-based interpretation ofFHR records, clinical records are, with few exceptions, read visually. The limited inter-observer agreement on the interpretation of FHR variables has been well documented.37 However, our experience has shown a high degree of inter-observer agreement in the classification of FHR patterns in one hour of recording. 3. Fetal heart rate algorithm to predict fetal asphyxia The need for a detailed algorithm for the interpretation of the FHR record is the most important outstanding issue. A matched case-control study was conducted in women with term pregnancies to demonstrate that a threshold of FHR patterns can be defined and that patterns based on one hour of FHR recording that are either "potentially predictive" or "predictive" for intrapartum fetal asphyxia can be determined. 38 A number of relevant observations emerged from this stUdy. The sensitivity of predictive and potentially predictive FHR patterns was good, identifying 75% of the cases with fetal asphyxia. In the 25% of cases not identified, the fetal asphyxia was mild. The positive predictive value of the "predictive FHR pattern" that occurred in 17% of the cases was very good. However, in these cases the fetal asphyxia was already moderate or severe. The positive predictive value of "potentially predictive FHR patterns" was very poor. These potentially predictive patterns accounted for over 50% of mild to moderate fetal asphyxia.
If an algorithm such as this is to be used, the FHR record must be continuously scored to identify predictive and, most importantly, potentially predictive patterns. If the objective is to prevent moderate and severe asphyxia, the clinician cannot wait for a predictive FHR pattern because by this point the fetal asphyxia is already moderate or severe. The key to avoiding moderate and severe fetal asphyxia lies in the intermediate FHR patterns expressed by the potentially predictive patterns in this algorithm that were associated with mild or moderate fetal asphyxia. Unless they can be clarified by supplementary tests, these potentially predictive FHR patterns represent a huge
The Current Crisis in Obstetrics
dilemma for the clinician. If the patter~ is ignored, there will be no intervention. In 9 cases out of 10, fetal asphyxia will be absent and intervention unnecessary. However, in the tenth case, fetal asphyxia will be present and will continue; this will account for at least 50% of the total occurrence of asphyxia. On the other hand, if the pattern were to be used as an indication for intervention, it would lead to unnecessary intervention in nine of ten cases.
4. Clinical management protocol In the development of clinical management protocols, the objective of fetal monitoring is to predict mild fetal asphyxia and prevent progression to moderate or severe fetal asphyxia with newborn cerebral dysfunction and brain damage. The window of opportunity for the prediction and diagnosis of mild fetal asphyxia will vary widely in relation to the diversity of fetal asphyxia. Determining the duration of this window in individual cases is difficult because of the limited information available about the duration, degree, and nature of the asphyxia and the quality of the fetal cardiovascular response. This makes the definition of a decision-delivery time in clinical management protocols difficult.
5. Surveillance of low-risk obstetric patients The final issue to be considered is a fetal surveillance protocol for low-risk obstetric patients, who account for approximately 25% of cases of fetal asphyxia. Current guidelines advocate the use of intermittent FHR auscultation in the surveillance of the low-risk obstetric patient, even though there are no randomized clinical trials to support the benefit of this procedure. If the goal of preventing fetal asphyxia is to be achieved, the intermediate potentially predictive FHR patterns must be identified. This requires the early recognition, by auscultation, of minimal baseline variability and late or prolonged decelerations. Even in a continuous FHR record, the inter-observer agreement in discriminating between moderate and minimal baseline FHR variability and between variable and late decelerations is low. It is not realistic to anticipate that intermittent auscultation can effectively determine FHR patterns in six 10-minute cycles over one hour to identify the onset of potentially predictive patterns. It is counterintuitive to assume that current fetal assessment protocols for low-risk obstetric patients are effective. Until these issues are resolved, it cannot be claimed that there is a single standard of care for the use of EFM in the prediction and diagnosis of fetal asphyxia. Individual health care workers will interpret FHR records in relation to the clinical circumstances in different ways.
WHERE WE ARE TODAY
The commitment of society and reproductive health care workers during the 20th century has led to a dramatic decrease of both maternal and perinatal mortality. During this same period there was little or no change in the prevalence of cerebral palsy.39 This can be attributed in part to our limited understanding of the multiple causes of cerebral palsy, including fetal asphyxia, in spite of the progress made in the research of this subject. Most investigators believe that EFM can be of value in the prediction of fetal asphyxia. Our experience in both term and preterm pregnancies suggests that interpretation of FHR patterns, supplemented with fetal blood gas and acid-base assessment, has led to selected intervention and the prevention of the progression of mild to moderate or severe fetal asphyxia in some cases. 40,41 This has likely contributed to a modest decrease in the number of cases of cerebral palsy due to fetal asphyxia in the term newborn, but has not been enough to influence the prevalence figures for cerebral palsy. Who Is Responsible for the Current Crisis in Obstetrics? The responsibility is not with the parents of children with motor and possibly mental disabilities, who need all the help society can provide to support these children and permit them to achieve the best possible quality of life within the constraints of their disability. Medical-legal action provides financial assistance to a few, but many never receive any assistance. Even those who do receive assistance may have to wait many years for a favourable decision; often, it is during those years that their need for financial aid is greatest.
Nor is the responsibility with the legal system. The methodology of the legal system is challenged by scientific uncertainty.42 In the absence of scientific proof, legal answers are determined on a balance of probabilities. However, a balance of probabilities must be distinguished from speculation. Lawyers can work only with current knowledge and the interpretation of that knowledge provided by health care workers who are considered to be experts in the field. The responsibility must rest with the health care disciplines that provide reproductive care and expert testimony. Our retrospective definition of the problem of fetal asphyxia has outstripped our ability to predict its occurrence with the accuracy society expects. Progress in research encourages us to assume that more is known about the cause of brain damage in the clinical setting than in fact is known. Similarly, health professionals, parents, and lawyers often assume current methods of prediction and diagnosis to be more effective than they actually are.
NOVEMBER]OGC NOVEMBRE 2005.
1035
COMMENTARY
We must continue to foster research and the growth of knowledge in this area. Granting agencies must not assume these problems are already resolved. At the same time, the limitations of our current knowledge must be recognized, or the mismatch between societal expectations of science and the reality may cripple the practice of obstetrics.
REFERENCES 1. Society of Obstetricians and Gynaecologists of Canada. Policy Statement No. 19: Task force on Cerebral Palsy and Neonatal Asphyxia. SOGC Clinical Practice Guidelines 1995;28. 2. Ranck JB, Windle WF. Brain damage in the monkey, macaca mulatta, by asphyxia neonatorum. Exp NeuroI1959;1:130-54. 3. Mallard EC, Gunn A], Williams CE,Johnston BM, Gluckman PD. Transient umbilical cord occlusion causes hippocampal damage in the fetal sheep. Am] ObstefGynecoI1992;167:1423-30. 4. Keunen H, Deutz NE, Van Reempts ]L, Hasaart TH. Transient umbilical cord occlusion in' late-gestation fetal sheep results in hippocampal damage but not in cerebral arteriovenous difference for nitrite, a stable end product of nitric oxide. J Soc Gynecol Investig 1999; 6: 120-6. 5. Williams CE, Gunn A], Mallard C, Gluckman PD. Outcome after ischemia in the developing sheep brain: an electro-encephalographic and histological study. Ann Neural 1992;31:14-21. 6. Myers RE. Four patterns of perinatal brain damage and their conditions of occurrence in primates. Adv Neurol 1975;10:223-34.
17. Mallard EC, Waldvogel HJ, Williams CE, Faull RL, Gluckman PD. Repeated asphyxia causes loss of striatal projection neurons in the fetal sheep brain. Neuroscience 1995;65:827-36. 18. De Haan HH, GunnA], Williams CE, Gluckman PD. Brief repeated umbilical cord occlusions cause sustained cytotoxic cerebral edema and focal infarcts in near-term fetal lambs. Pediatt Res 1997;41:9&-104. 19. Garnier Y, Coumans A, Berger R,]ensen A, Hasaart THM. Endotoxemia severely affects circulation during normoxia and asphyxia in immature fetal sheep.] Soc Gynecol Investig 2001;8:134-42. 20. Dalitz P, Harding R, Rees SM, Cock ML. Prolonged reductions in placental blood flow and cerebral oxygen delivery in preterm fetal sheep exposed to endotoxin: Possible factors in white matter injury after acute infection.] Soc Gynecol Investig 2003;10:283-90 21. DuncanJR, Cock ML, Scheerlinck]Y, Westcott KT, McLean C, Harding R, et al. White matter injury after repeated endotoxin exposure in the preterm ovine fetus. Pediatr Res 2002;52:941-9. 22. Mallard C, Welin A, Peebles D, Hagberg H, Kjellmar 1. White matter injury following systemic endotoxemia or asphyxia in the fetal sheep. Neurochem Res 2003;28:215-23. 23. Mallard EC, Rees S, Stringer M, Cock MI~, Harding R. Effects of chronic placental insufficiency on brain development in fetal sheep. Pediatr Res 1998; 43:262-70. 24. Duncan ]R, Cock ML, Harding R, Rees SM. Relation between damage to the placenta and the fetal brain after late-gestation placental embolization and fetal growth restriction in sheep. Am J Obstet Gynecol 2000;183: 1013--22.
7. Gunn AJ, Parer JT, Mallard EC, Williams CE, Gluckman PD. Cerebral histologic and electrocorticographic changes after asphyxia in fetal sheep. Pediatr Res 1992;31 :48&-91.
25. Low]A, Lindsay BG, Derrick E]. Threshold of metabolic acidosis associated with newborn complications. Am J Obstet Gynecol 1997;177:1391-4.
8. Ikeda T, Murata Y, Quilligan EJ, Choi BH, Parer JT, Doi S, et al. Physiologic and histologic changes in near-term fetal lambs exposed to asphyxia by partial umbilical cord occlusion. Am] Obstet Gynecol 1998;178:24-32.
26. Low JA. Intrapartum fetal asphyxia: definition, diagnosis, and classification. Am J Obstet Gynecol .1997;76:957-9.
9. Richardson BS, Rurak D, PatrickJE, Homan], Carmichael L. Cerebral oxidative metabolism during sustained hypoxaemia in fetal sheep.] Dev PhysioI1989;11:37-43. 10. Jensen A, Roman C, Rudolph AM. Effects of reducing uterine blood flow on fetal blood flow distribution and oxygen delivery. J Dev Physio! 1991;15:309-23. 11. Ball RH, Parer ]T, Caldwell LE, Johnson]. Regional blood flow and metabolism in ovine fetuses during severe cord occlusion. Am] Obstet GynecoI1994;171:1549-55. 12. Jensen A, Lang U. Foetal circulatory responses to arrest of uterine blood flow in sheep: effects of chemical sympathectomy. J Dev Physiol 1992;17:75-86. 13. Mallard EC, Williams CE,Johnston BM, Gluckman PD. Increased vulnerability to neuronal damage after umbilical cord occlusion in fetal sheep with advancing gestation. AmJ Obstet GynecoI1994;170:206-14. 14. Keunen H, Blanco CE, van Reempts JL, Hasaart TH. Absence of neuronal damage after umbilical cord occlusion of 10,15, and 20 minutes in midgestation fetal sheep. Am J Obstet GynecoI1997;176:515-20. 15. Benn~t L, Rossenrode S, Gunning MI, Gluckman PD, Gunn AJ. The cardiovascular and cerebrovascular responses of the immature fetal sheep to acute umbilical cord occlusion.] Physiol (Lond) 1999;517:247-57. 16. Mallard EC, Williams CE, Gunn A], Gunning MI, Gluckman PD. Frequent episodes of brief ischemia sensitize the fetal sheep brain to neuronal loss and induce striatal injury. Pediatr Res 1993;33:61-5.
1036 • NOVEMBER]OGC NOVEMBRE 2005
27. Low]A, Simpson LL, Tonni G, Chamberlain S. Limitations in the clinical prediction of intrapartum fetal asphyxia. Am] Obstet Gynecol 1995;172:801-4. 28. Low]A, Simpson LL, Ramsey DA. The clinical diagnosis of asphyxia responsible for brain damage in the human fetus. Am] Obstet Gynecol 1992;167:11-5. 29. Hon EH. The electronic evaluation of the fetal heart rate. Am J Obstet GynecoI1958;75:1215-30. 30. NeilsonJP. EFM alone vs. intermittent auscultation in labor (revised 04 May 1994). In: Kelrse MJNC, Renfrew M], NeilsonJP, Crowther C, editors. Pregnancy and Childbirth Module. In: The Cochrane Pregnancy and Childbirth Database. The Cochrane Collaborative Issue 2. Oxford: Update Software;1995. 31. Neilson ]P. EFM + scalp sampling vs. intermittent auscultation in labor (revised 04 May 1994). In Keirse M]NC, Renfrew MJ, Neilson]P, Crowther C, editors. Pregnancy and Childbirth Module. In The Cochrane Pregnancy and Childbirth Database: The Cochrane Collaboration Issue 2. Oxford: Update Software; 1995. 32. Society of Obstetricians and Gynaecologists of Canada. Guidelines for fetal health surveillance in labour. SOGC Clinical Practice Guidelines. No. 112; March 2001. 33. American College of Obstetrics and Gynecology. ACOG Technical Bulletin. Fetal heart rate patterns: monitoring, interpretation, and management. Number 207; July 1995. Int] Gynaecol Obstet 1995;5:65-74. 34. Royal College of Obstetricians and Gynaecologists. The use of electronic fetal monitoring. Evidence-based Clinical Guideline. No.8; May 2001.
The Current Crisis in Obstetrics
35. National Institute of Child Health and Human Development Research Planning Workshop. Electronic fetal heart rate monitoring research guidelines for interpretation. 36. Freeman R. Problems with intrapartum fetal heart rate monitoring interpretation and patient management. Obstet Gynecol 2002;100:813-26. 37. Paneth N, Bommarito M, Stricker]. Electronic fetal monitoring and later outcome. Clin Invest Med 1993;16:159-65. 38. Low] A, Victory R, Derrick EJ. Predictive value of electronic fetal monitoring for intrapartum fetal asphyxia with metabolic acidosis. Obstet Gynecol 1999;93:285-91.
39. Clark SL, Hankins GDV. Temporal and demographic trends in cerebral palsy-Fact and fiction. Am] Obstet GynecoI2003;188:628-33. 40. Low]A, Pickersgill H, Killen HL, Derrick EJ. The prediction and prevention of intrapartum fetal asphyxia in term pregnancies. Am] Obstet GynecoI2001;184:724--30. 41. Low]A, Killen HL, Derrick EJ. The prediction and prevention of intrapartum fetal asphyxia in pre term pregnancies. Am] Obstet Gynecol 2002; 186:279-82. 42. Snell v. Farrell, (1990) 2 S. C. R. 311.
NOVEMBER JOGC NOVEMBRE 2005.
1037
The Current Crisis in Obstetrics James A. Low, MD Department of Obstetrics and Gynaecology, Queen's University, Kingston ON
Abstract
une conclusion, au sujet du moment ou sont survenues les lesions cerebrales, en fonction de la preponderance des probabilites.
Of the issues leading to legal actions in obstetrics, the most important are events occurring before delivery that are deemed to account for the birth of a physically or mentally challenged child.
Bien qu'il so it d'une certaine utilite, la determination du risque clinique au moyen de la surveillance de la frequence cardiaque fcetale (FCF) peut generer des resultats faux positifs en matiere de prediction de I'asphyxie intra-uterine. Le probleme, dans Ie cas de la surveillance de la FCF, c'est I'absence d'un algorithme detaille pour I'interpretation des traces de FCF comptant des recommandations appropriees en matiere de prise en charge. Jusqu'a ce qu'un tel algorithme soit elabore, on ne peut s'attendre a ce que les intervenants en sante reagissent de fayon uniforme aux traces de frequence cardiaque fcetale.
In determining causation in the clinical setting, the diagnosis of fetal asphyxia can be made using blood gas and acid-base assessment. However, there are many subsidiary questions that in most cases cannot be answered, including when the asphyxia began, the severity and nature of the asphyxia during the exposure, the quality of the cardiovascular compensation, and when the brain damage occurred. When scientific proof is not available, the dilemma for the court is the requirement to reach a conclusion about the timing of brain damage on the balance of probabilities. Although it is of value, clinical risk scoring using fetal heart rate (FHR) monitoring may result in false positive predictions of fetal asphyxia. The problem in FHR monitoring is the lack of a detailed algorithm for the interpretation of FHR patterns with appropriate recommendations for management. Until such an algorithm is developed, health care workers cannot be expected to respond·to fetal heart rate patterns consistently. Responsibility for the crisis in obstetrics must rest with the members of the health care disciplines who provide expert testimony. Progress made in research encourages us to assume that more is known about the causes of brain damage in the clinical setting than in fact is known. Similarly, health care professionals, parents, and lawyers often assume current methods of prediction and diagnosis to be more effective than they actually are.
Resume Les evenements qui surviennent avant I'accouchement et qui sont tenus pour responsables de la naissance d'un enfant presentant une deficience physique ou mentale constituent les plus importants motifs de poursuites judiciaires dans Ie domaine de I'obstetrique. Lorsque vient Ie temps de determiner les causes d'un tel evenement en milieu clinique, il est possible de poser un diagnostic d'asphyxie intra-uterine au moyen d'une evaluation en fonction de la gazometrie et de I'acidite. Toutefois, il subsiste de nombreuses questions incidentes qui, dans la plupart des cas, ne peuvent etre elucidees, y compris la determination du moment a partir duquel I'asphyxie a debute, la gravite et la nature de I'asphyxie au cours de I'exposition, la qualite de la compensation cardiovasculaire, ainsi que la determination du moment ou sont survenues les lesions cerebrales. En I'absence de preuves scientifiques, les tribunaux sont confrontes au fait de devoir tirer Key Words: Fetal asphyxia, brain damage, medical legal Competing Interests: None declared. Received on March 21 , 2005 Accepted on July 21 , 2005
La responsabilite, quant a la crise que connait I'obstetrique, doit etre assumee par les membres des disciplines de la sante qui fournissent des temoignages d'expert. Les progres realises dans Ie domaine de la recherche nous poussent a presumer que les connaissances au sujet des causes des lesions cerebrales sont superieures a ce qu'eUes sont en realite. De fayon similaire, les profession nels de la sante, les parents et les avocats presument souvent que les methodes actuelles de prediction et de diagnostic sont plus efficaces qu'elles ne Ie sont vraiment.
J Obstet Gynaecol Can 2005;27(11):1031-1037
INTRODUCTION
I
n 2004, the Canadian Medical Protective Association fees in Ontario for physicians practising obstetrics ($86244) were 10 times the average of fees for all health care disciplines ($8783). These fees reflect the number of new fJles opened, threats of medico-legal difficulty, legal actions commenced, legal actions proceeding to trial, and judgements for the plaintiff. Does this imply that physicians providing obstetric care are 10 times less competent than physicians in other disciplines? That they are10 times more likely to make mistakes? That they care 10 times less for patient welfare? If we assume that these statements are not true, then what is the problem? By far the most important reasons for such medical-legal actions are events occurring before delivery that are considered to account for a child's being physically and possibly mentally challenged. 1 Two issues arising from these legal actions are causation and standard of care. The cause receiving most attention is fetal asphyxia. The standard of care is usually assessed by the paradigm of fetal monitoring before and during labour, which is designed to predict and establish a diagnosis of fetal asphyxia.
NOVEMBER JOGe NOVEMBRE 2005.
1031
COMMENTARY
The objective of this review is to examine our current understanding of the relationship between fetal asphyxia and brain damage, and the characteristics of the current paradigm for the prediction, diagnosis, and management of fetal asphyxia. FETAL ASPHYXIA AS A CAUSE OF BRAIN DAMAGE
Clarifying the significance of fetal asphyxia as a cause of brain damage began in the mid-20th century when the systematic examination of the effect of asphyxia and ischemia on the fetus began in the research laboratory. These studies have provided the foundation for our understanding of the relationship between fetal asphyxia and brain damage. The initial studies demonstrated that total fetal asphyxia lasting more than 12 minutes 2- 5 and partial fetal asphyxia lasting more than 60 minutes 6- 8 may cause brain damage, with severe metabolic acidosis and hypotension found consistently before brain damage occurred. The outcome of a uniform single episode of fetal asphyxia has been strikingly variable, ranging from no brain damage in many fetuses to brain damage in some and to fetal death in a few. This variability of outcome is due in large part to the fetus's' compensatory cardiovascular response to asphyxia. There is a redistribution of cardiac output with increased blood flow to the brain, heart, and adrenals: 9- 12 the balance between the quality of the fetal' cardiovascular response and the degree and duration of fetal asphyxia may determine whether or not the asphyxia leads to brain damage. However, as studies have continued, this relationship has become more complicated. The immature fetus differs from the mature fetus. Total cord occlusion studies indicate that the immature fetus will survive a longer period of asphyxia. Following a more prolonged episode of asphyxia, this capacity to survive exposes the immature fetus to sudden decompensation with profound hypotension and hypoperfusion. 13- 15 Fetal asphyxia may be a recurrent event, and repeated episodes may have a cumulative effect with brain damage even if individual episodes would not cause brain damage. 16- 18 Intrauterine infection is a confounding factor. Coliform endotoxemia, with release of circulating proinflammatory cytokines, will compromise fetal cardiovascular function. The mechanism of fetal cardiovascular compensation is not effective against the hypoxemia associated with endotoxemia or a concurrent exposure to fetal asphyxia. 19- 22 Brain damage that follows fetal asphyxia with concurrent fetal infection may develop because of both increased sensitivity to hypoxemia-ischemia and the direct effect of cytokines in the brain.
1032 • NOVEMBER}OGC NOVEMBRE 2005
Recent laboratory studies of placental insufficiency suggest an entirely different mechanism of brain damage. Placental insufficiency induced for 20 to 30 days in sheep, causing fetal hypoxemia without metabolic acidosis, resulted in brain damage prominent in the cerebral white matter. 23,24 As these studies have continued, the complexity of the relationship between fetal asphyxia and brain damage has become apparent. FETAL ASPHYXIA AS A CAUSE OF BRAIN DAMAGE IN THE CLINICAL SETTING
The introduction of microelectrode blood gas systems permitted clinical studies that could evaluate fetal asphyxia at the time of delivery. Intrapartum fetal asphyxia must be progressive, leading to a metabolic acidosis, to be ofpathological significance. The threshold of a metabolic acidosis at delivery beyond which cerebral dysfunction may occur has been determined to be an umbilical artery base deficit greater than 12 mmol/L.25 Thus a blood gas and acid-base assessment at delivery that shows a significant metabolic acidosis confirms that fetal asphyxia has occurred. Because most methods used in the animal laboratory to assess asphyxia are not available in the clinical setting, the clinical classification of asphyxia as mild, moderate, or severe is based on the presence of metabolic acidosis (to confirm the occurrence of asphyxia) with measures of neonatal encephalopathy and other organ system complications (to express the severity of the asphyxia).26 This classification is of prognostic value, with significant newborn morbidity and brain damage occurring in some newborns with either moderate or severe fetal asphyxia. Although an umbilical cord blood gas and acid-base assessment at delivery can confirm that asphyxia has occurred, the following questions are relevant but may not have answers.
1. When did fetal asphyxia begin? A growing body of indirect and direct evidence points to the importance of antepartum fetal asphyxia as a cause of brain damage and deficits in surviving children. Although the prevalence of intrapartum fetal asphyxia as determined at delivery has been established, the duration and nature (i.e., continuous or intermittent) of the asphyxia in most cases is not known. Since the duration of the asphyxia cannot be determined, it is not known how often the asphyxia identified at delivery may have begun before the onset of labour. Since the natilre of the asphyxia cannot be determined, it is not known how often the asphyxia identified at delivery represents the last in a series of episodes of asphyxia that may have begun before the onset of labour. When asphyxia is limited to the intrapartum period, the time when the asphyxia began and the nature of the asphyxia can rarely be determined.
The Current Crisis in Obstetrics
2. What was the severity and nature of the asphyxia? Because the blood gas and acid-base status of the fetus cannot be measured continuously during labour, the severity and nature of the asphyxial exposure is rarely known. Asphyxia during labour is often perceived to be either acute (almost total) asphyxia or partial asphyxia on the basis of the initial research models that contributed to current understanding of the relationship between fetal asphyxia and brain damage. These and subsequent models were achieved by careful control of induced maternal hypoxemia, reduced utero placental blood flow, umbilical cord blood flow, or carotid artery blood flow, and such circumstances are unlikely to be duplicated in the clinical setting. This suggests that asphyxia occurs like a switch with off, mild, moderate, and severe settings, but the clinical setting is more likely to simulate a dimmer switch. 3. What was the quality of the fetal cardiovascular compensation? Without continuous measures of fetal blood pressure and organ blood flow throughout labour, the quality of the fetal cardiovascular compensation in response to fetal asphyxia is not known. Lacking this information, and understanding the complexity of the relationship between fetal asphyxia and brain damage, any speculation about the sequence of events prior to delivery will be fundamentally imprecise. 4. When did the brain damage occur? Accurately determining when brain damage occurred is impossible in the absence of information about when the asphyxia began, the nature and severity of the asphyxial episode, and the quality of the fetal cardiovascular compensation. Indirect' measures such as clinical sentinel events, abnormal FHR patterns, and ultrasound, computerized tomography (C1) scans, and magnetic resonance imaging (MRI) studies provide indirect markers in some cases. However, these observations do not provide specific insight into when the brain damage has occurred. An umbilical cord blood gas and acid-base assessment at delivery will confirm that an asphyxial exposure has occurred, and the asphyxial exposure can be classified as mild, moderate, or severe on the basis of the neonatal course. However, it is rare that an obstetric expert can give an accurate opinion about the sequence of events before delivery and specifically when the brain damage has occurred. In the case of a legal action following delivery of a brain damaged baby, the dilemma for the court is the requirement to reach a conclusion about the timing of brain damage due to fetal asphyxia on the balance of probabilities when scientific proof is not available.
STANDARD OF CARE FOR THE PREDICTION AND DIAGNOSIS OF FETAL ASPHYXIA
The diagnosis of fetal asphyxia can be confirmed by means of periodic fetal scalp blood sampling during labour or cord blood sampling at delivery for a blood gas and acid-base assessment. To define a standard of care, we need criteria to identify the fetus at enough risk for fetal asphyxia during labour to justify an intervention for fetal blood sampling for a fetal blood gas and acid-base assessment. A combination of clinical risk scoring and FHR surveillance has been widely used to identify the fetus at risk of asphyxia; however, the shortcomings of each element have become evident with increasing clinical experience. Clinical Risk Scoring The limitations of clinical risk scoring have been demonstrated in several studies. In our experience, 23% to 40% of fetal asphyxia occurred in pregnancies with no clinical risk factors. 27- 28 The term "low risk" based on clinical markers cannot be applied to the risk of fetal asphyxia during labour.
In those cases in which clinical risk factors were present, a wide range of clinical complications determined risk, and no single risk factor demonstrated a strong association with intrapartum fetal asphyxia. The positive predictive value for both antepartum and intrapartum clinical risk factors for intrapartum fetal asphyxia was 3%.27 Thus, clinical risk scoring has a very high rate of false positive prediction of intrapartum fetal asphyxia. Electronic Fetal Heart Rate Monitoring A 1958 publication by Edward Hon 29 created an expectation that electronic FHR monitoring (EFM) would be useful in the prediction of intrapartum fetal asphyxia. Observations subsequently supported the contention that EFM could be a useful screening test for the prediction of intrapartum fetal asphyxia. Our clinical experience paralleled that of other investigators in this field with anecdotal examples of an association between abnormal FHR patterns and fetal asphyxia with a range of outcomes. On the basis of such experience, the use ofEFM expanded rapidly in the 1970s.
There are two requirements for a screening test. First, the clinical problem must justify intervention. Intrapartum fetal asphyxia is important and in selected circumstances justifies intervention. Second, the benefits of the test must outweigh the harm. We recognized in the late 1970s that this had not been determined. Well-designed, randomized controlled trials are the current standard for providing a measure of the true risks and benefits of a medical intervention. There have been no randomized clinical trials to compare "no fetal heart rate monitoring" with "intermittent fetal heart rate auscultation." Nine
NOVEMBER]OGC NOVEMBRE 2005.
1033
COMMENTARY
randomized clinical trials, three with electronic fetal monitoring alone and six with electronic fetal monitoring and scalp blood sampling, have been analyzed in the Cochrane Pregnancy and Childbirth Database.30,31 The randomized clinical trials comparing intermittent auscultation and continuous EFM have not provided consistent evidence that EFM was associated with a decrease in fetal and newborn morbidity. The randomized clinical trials have made an important contribution, confirming the occurrence of false positive interpretation of EFM, with consequent unnecessary interventions. These studies have demonstrated that EFM has been associated with an increased incidence of Caesarean section for fetal distress and dystocia, operative delivery, and general anaesthesia compared with intermittent auscultation. Faced with the available evidence, national organizations began to prepare consensus papers on the subject of fetal surveillance during labour. Clinical guidelines have been recently published by the Society of Obstetricians and Gynaecologists of Canada (SOGq, 32 the American College of Obstetricians and Gynecologists (ACOG),33 and the Royal College of Obstetricians and Gynaecologists (RCOG).34 These guidelines, prepared by recognized experts in the field, reflected the best evidence available at the time of publication. What is missing from all the current guidelines is a specific algorithm for the interpretation of FHR patterns. The SOGC and the ACOG guidelines classify FHR patterns as reassuring and non-reassuring. Detailed criteria and duration are not noted. The RCOG guidelines have defined EFM traces as normal, suspicious, and pathological. No guidelines have provided information about the sensitivity, specificity, and predictive value of the patterns as defined. This issue was addressed by a National Institutes of Health (NIH) research-planning workshop in 1997. 35 Although all members of the workshop agreed that EFM was of value, there was no consensus regarding strict guidelines for clinical management using FHR patterns. The position expressed was that many fetuses have FHR tracings that are neither totally normal nor so severely abnormal that the fetus is at risk of morbidity or mortality. The workshop concluded that developing evidence-based algorithms for management will require further research. Recently, this view has been expressed again. 36 Until such specific algorithms are developed, health care workers responsible for the care of obstetric patients cannot be expected to respond to abnormal FHR patterns consistently.
1034 • NOVEMBER]OGC NOVEMBRE 2005
Clinical In terpre.ta tion of the FHR Record The following issues remain to be resolved for the interpretation of a FHR record.
1. Classification of FHR variables Many definitions of the individual FHR variables (baseline FHR, bal'eline FHR variability, accelerations and decelerations) have been provided. However, differences in the criteria for classification remain, particularly for decelerations. While such a consensus is being developed, criteria should always be clearly defined and consistently used. 2. Inter-observer reliability Although progress is being made in the computer-based interpretation ofFHR records, clinical records are, with few exceptions, read visually. The limited inter-observer agreement on the interpretation of FHR variables has been well documented.37 However, our experience has shown a high degree of inter-observer agreement in the classification of FHR patterns in one hour of recording. 3. Fetal heart rate algorithm to predict fetal asphyxia The need for a detailed algorithm for the interpretation of the FHR record is the most important outstanding issue. A matched case-control study was conducted in women with term pregnancies to demonstrate that a threshold of FHR patterns can be defined and that patterns based on one hour of FHR recording that are either "potentially predictive" or "predictive" for intrapartum fetal asphyxia can be determined. 38 A number of relevant observations emerged from this stUdy. The sensitivity of predictive and potentially predictive FHR patterns was good, identifying 75% of the cases with fetal asphyxia. In the 25% of cases not identified, the fetal asphyxia was mild. The positive predictive value of the "predictive FHR pattern" that occurred in 17% of the cases was very good. However, in these cases the fetal asphyxia was already moderate or severe. The positive predictive value of "potentially predictive FHR patterns" was very poor. These potentially predictive patterns accounted for over 50% of mild to moderate fetal asphyxia.
If an algorithm such as this is to be used, the FHR record must be continuously scored to identify predictive and, most importantly, potentially predictive patterns. If the objective is to prevent moderate and severe asphyxia, the clinician cannot wait for a predictive FHR pattern because by this point the fetal asphyxia is already moderate or severe. The key to avoiding moderate and severe fetal asphyxia lies in the intermediate FHR patterns expressed by the potentially predictive patterns in this algorithm that were associated with mild or moderate fetal asphyxia. Unless they can be clarified by supplementary tests, these potentially predictive FHR patterns represent a huge
The Current Crisis in Obstetrics
dilemma for the clinician. If the patter~ is ignored, there will be no intervention. In 9 cases out of 10, fetal asphyxia will be absent and intervention unnecessary. However, in the tenth case, fetal asphyxia will be present and will continue; this will account for at least 50% of the total occurrence of asphyxia. On the other hand, if the pattern were to be used as an indication for intervention, it would lead to unnecessary intervention in nine of ten cases.
4. Clinical management protocol In the development of clinical management protocols, the objective of fetal monitoring is to predict mild fetal asphyxia and prevent progression to moderate or severe fetal asphyxia with newborn cerebral dysfunction and brain damage. The window of opportunity for the prediction and diagnosis of mild fetal asphyxia will vary widely in relation to the diversity of fetal asphyxia. Determining the duration of this window in individual cases is difficult because of the limited information available about the duration, degree, and nature of the asphyxia and the quality of the fetal cardiovascular response. This makes the definition of a decision-delivery time in clinical management protocols difficult.
5. Surveillance of low-risk obstetric patients The final issue to be considered is a fetal surveillance protocol for low-risk obstetric patients, who account for approximately 25% of cases of fetal asphyxia. Current guidelines advocate the use of intermittent FHR auscultation in the surveillance of the low-risk obstetric patient, even though there are no randomized clinical trials to support the benefit of this procedure. If the goal of preventing fetal asphyxia is to be achieved, the intermediate potentially predictive FHR patterns must be identified. This requires the early recognition, by auscultation, of minimal baseline variability and late or prolonged decelerations. Even in a continuous FHR record, the inter-observer agreement in discriminating between moderate and minimal baseline FHR variability and between variable and late decelerations is low. It is not realistic to anticipate that intermittent auscultation can effectively determine FHR patterns in six 10-minute cycles over one hour to identify the onset of potentially predictive patterns. It is counterintuitive to assume that current fetal assessment protocols for low-risk obstetric patients are effective. Until these issues are resolved, it cannot be claimed that there is a single standard of care for the use of EFM in the prediction and diagnosis of fetal asphyxia. Individual health care workers will interpret FHR records in relation to the clinical circumstances in different ways.
WHERE WE ARE TODAY
The commitment of society and reproductive health care workers during the 20th century has led to a dramatic decrease of both maternal and perinatal mortality. During this same period there was little or no change in the prevalence of cerebral palsy.39 This can be attributed in part to our limited understanding of the multiple causes of cerebral palsy, including fetal asphyxia, in spite of the progress made in the research of this subject. Most investigators believe that EFM can be of value in the prediction of fetal asphyxia. Our experience in both term and preterm pregnancies suggests that interpretation of FHR patterns, supplemented with fetal blood gas and acid-base assessment, has led to selected intervention and the prevention of the progression of mild to moderate or severe fetal asphyxia in some cases. 40,41 This has likely contributed to a modest decrease in the number of cases of cerebral palsy due to fetal asphyxia in the term newborn, but has not been enough to influence the prevalence figures for cerebral palsy. Who Is Responsible for the Current Crisis in Obstetrics? The responsibility is not with the parents of children with motor and possibly mental disabilities, who need all the help society can provide to support these children and permit them to achieve the best possible quality of life within the constraints of their disability. Medical-legal action provides financial assistance to a few, but many never receive any assistance. Even those who do receive assistance may have to wait many years for a favourable decision; often, it is during those years that their need for financial aid is greatest.
Nor is the responsibility with the legal system. The methodology of the legal system is challenged by scientific uncertainty.42 In the absence of scientific proof, legal answers are determined on a balance of probabilities. However, a balance of probabilities must be distinguished from speculation. Lawyers can work only with current knowledge and the interpretation of that knowledge provided by health care workers who are considered to be experts in the field. The responsibility must rest with the health care disciplines that provide reproductive care and expert testimony. Our retrospective definition of the problem of fetal asphyxia has outstripped our ability to predict its occurrence with the accuracy society expects. Progress in research encourages us to assume that more is known about the cause of brain damage in the clinical setting than in fact is known. Similarly, health professionals, parents, and lawyers often assume current methods of prediction and diagnosis to be more effective than they actually are.
NOVEMBER]OGC NOVEMBRE 2005.
1035
COMMENTARY
We must continue to foster research and the growth of knowledge in this area. Granting agencies must not assume these problems are already resolved. At the same time, the limitations of our current knowledge must be recognized, or the mismatch between societal expectations of science and the reality may cripple the practice of obstetrics.
REFERENCES 1. Society of Obstetricians and Gynaecologists of Canada. Policy Statement No. 19: Task force on Cerebral Palsy and Neonatal Asphyxia. SOGC Clinical Practice Guidelines 1995;28. 2. Ranck JB, Windle WF. Brain damage in the monkey, macaca mulatta, by asphyxia neonatorum. Exp NeuroI1959;1:130-54. 3. Mallard EC, Gunn A], Williams CE,Johnston BM, Gluckman PD. Transient umbilical cord occlusion causes hippocampal damage in the fetal sheep. Am] ObstefGynecoI1992;167:1423-30. 4. Keunen H, Deutz NE, Van Reempts ]L, Hasaart TH. Transient umbilical cord occlusion in' late-gestation fetal sheep results in hippocampal damage but not in cerebral arteriovenous difference for nitrite, a stable end product of nitric oxide. J Soc Gynecol Investig 1999; 6: 120-6. 5. Williams CE, Gunn A], Mallard C, Gluckman PD. Outcome after ischemia in the developing sheep brain: an electro-encephalographic and histological study. Ann Neural 1992;31:14-21. 6. Myers RE. Four patterns of perinatal brain damage and their conditions of occurrence in primates. Adv Neurol 1975;10:223-34.
17. Mallard EC, Waldvogel HJ, Williams CE, Faull RL, Gluckman PD. Repeated asphyxia causes loss of striatal projection neurons in the fetal sheep brain. Neuroscience 1995;65:827-36. 18. De Haan HH, GunnA], Williams CE, Gluckman PD. Brief repeated umbilical cord occlusions cause sustained cytotoxic cerebral edema and focal infarcts in near-term fetal lambs. Pediatt Res 1997;41:9&-104. 19. Garnier Y, Coumans A, Berger R,]ensen A, Hasaart THM. Endotoxemia severely affects circulation during normoxia and asphyxia in immature fetal sheep.] Soc Gynecol Investig 2001;8:134-42. 20. Dalitz P, Harding R, Rees SM, Cock ML. Prolonged reductions in placental blood flow and cerebral oxygen delivery in preterm fetal sheep exposed to endotoxin: Possible factors in white matter injury after acute infection.] Soc Gynecol Investig 2003;10:283-90 21. DuncanJR, Cock ML, Scheerlinck]Y, Westcott KT, McLean C, Harding R, et al. White matter injury after repeated endotoxin exposure in the preterm ovine fetus. Pediatr Res 2002;52:941-9. 22. Mallard C, Welin A, Peebles D, Hagberg H, Kjellmar 1. White matter injury following systemic endotoxemia or asphyxia in the fetal sheep. Neurochem Res 2003;28:215-23. 23. Mallard EC, Rees S, Stringer M, Cock MI~, Harding R. Effects of chronic placental insufficiency on brain development in fetal sheep. Pediatr Res 1998; 43:262-70. 24. Duncan ]R, Cock ML, Harding R, Rees SM. Relation between damage to the placenta and the fetal brain after late-gestation placental embolization and fetal growth restriction in sheep. Am J Obstet Gynecol 2000;183: 1013--22.
7. Gunn AJ, Parer JT, Mallard EC, Williams CE, Gluckman PD. Cerebral histologic and electrocorticographic changes after asphyxia in fetal sheep. Pediatr Res 1992;31 :48&-91.
25. Low]A, Lindsay BG, Derrick E]. Threshold of metabolic acidosis associated with newborn complications. Am J Obstet Gynecol 1997;177:1391-4.
8. Ikeda T, Murata Y, Quilligan EJ, Choi BH, Parer JT, Doi S, et al. Physiologic and histologic changes in near-term fetal lambs exposed to asphyxia by partial umbilical cord occlusion. Am] Obstet Gynecol 1998;178:24-32.
26. Low JA. Intrapartum fetal asphyxia: definition, diagnosis, and classification. Am J Obstet Gynecol .1997;76:957-9.
9. Richardson BS, Rurak D, PatrickJE, Homan], Carmichael L. Cerebral oxidative metabolism during sustained hypoxaemia in fetal sheep.] Dev PhysioI1989;11:37-43. 10. Jensen A, Roman C, Rudolph AM. Effects of reducing uterine blood flow on fetal blood flow distribution and oxygen delivery. J Dev Physio! 1991;15:309-23. 11. Ball RH, Parer ]T, Caldwell LE, Johnson]. Regional blood flow and metabolism in ovine fetuses during severe cord occlusion. Am] Obstet GynecoI1994;171:1549-55. 12. Jensen A, Lang U. Foetal circulatory responses to arrest of uterine blood flow in sheep: effects of chemical sympathectomy. J Dev Physiol 1992;17:75-86. 13. Mallard EC, Williams CE,Johnston BM, Gluckman PD. Increased vulnerability to neuronal damage after umbilical cord occlusion in fetal sheep with advancing gestation. AmJ Obstet GynecoI1994;170:206-14. 14. Keunen H, Blanco CE, van Reempts JL, Hasaart TH. Absence of neuronal damage after umbilical cord occlusion of 10,15, and 20 minutes in midgestation fetal sheep. Am J Obstet GynecoI1997;176:515-20. 15. Benn~t L, Rossenrode S, Gunning MI, Gluckman PD, Gunn AJ. The cardiovascular and cerebrovascular responses of the immature fetal sheep to acute umbilical cord occlusion.] Physiol (Lond) 1999;517:247-57. 16. Mallard EC, Williams CE, Gunn A], Gunning MI, Gluckman PD. Frequent episodes of brief ischemia sensitize the fetal sheep brain to neuronal loss and induce striatal injury. Pediatr Res 1993;33:61-5.
1036 • NOVEMBER]OGC NOVEMBRE 2005
27. Low]A, Simpson LL, Tonni G, Chamberlain S. Limitations in the clinical prediction of intrapartum fetal asphyxia. Am] Obstet Gynecol 1995;172:801-4. 28. Low]A, Simpson LL, Ramsey DA. The clinical diagnosis of asphyxia responsible for brain damage in the human fetus. Am] Obstet Gynecol 1992;167:11-5. 29. Hon EH. The electronic evaluation of the fetal heart rate. Am J Obstet GynecoI1958;75:1215-30. 30. NeilsonJP. EFM alone vs. intermittent auscultation in labor (revised 04 May 1994). In: Kelrse MJNC, Renfrew M], NeilsonJP, Crowther C, editors. Pregnancy and Childbirth Module. In: The Cochrane Pregnancy and Childbirth Database. The Cochrane Collaborative Issue 2. Oxford: Update Software;1995. 31. Neilson ]P. EFM + scalp sampling vs. intermittent auscultation in labor (revised 04 May 1994). In Keirse M]NC, Renfrew MJ, Neilson]P, Crowther C, editors. Pregnancy and Childbirth Module. In The Cochrane Pregnancy and Childbirth Database: The Cochrane Collaboration Issue 2. Oxford: Update Software; 1995. 32. Society of Obstetricians and Gynaecologists of Canada. Guidelines for fetal health surveillance in labour. SOGC Clinical Practice Guidelines. No. 112; March 2001. 33. American College of Obstetrics and Gynecology. ACOG Technical Bulletin. Fetal heart rate patterns: monitoring, interpretation, and management. Number 207; July 1995. Int] Gynaecol Obstet 1995;5:65-74. 34. Royal College of Obstetricians and Gynaecologists. The use of electronic fetal monitoring. Evidence-based Clinical Guideline. No.8; May 2001.
The Current Crisis in Obstetrics
35. National Institute of Child Health and Human Development Research Planning Workshop. Electronic fetal heart rate monitoring research guidelines for interpretation. 36. Freeman R. Problems with intrapartum fetal heart rate monitoring interpretation and patient management. Obstet Gynecol 2002;100:813-26. 37. Paneth N, Bommarito M, Stricker]. Electronic fetal monitoring and later outcome. Clin Invest Med 1993;16:159-65. 38. Low] A, Victory R, Derrick EJ. Predictive value of electronic fetal monitoring for intrapartum fetal asphyxia with metabolic acidosis. Obstet Gynecol 1999;93:285-91.
39. Clark SL, Hankins GDV. Temporal and demographic trends in cerebral palsy-Fact and fiction. Am] Obstet GynecoI2003;188:628-33. 40. Low]A, Pickersgill H, Killen HL, Derrick EJ. The prediction and prevention of intrapartum fetal asphyxia in term pregnancies. Am] Obstet GynecoI2001;184:724--30. 41. Low]A, Killen HL, Derrick EJ. The prediction and prevention of intrapartum fetal asphyxia in pre term pregnancies. Am] Obstet Gynecol 2002; 186:279-82. 42. Snell v. Farrell, (1990) 2 S. C. R. 311.
NOVEMBER JOGC NOVEMBRE 2005.
1037