Neurologically Impaired Babies?

Eldon L. Boisseau

Introduction

Each year, millions of dollars are transmitted from health care providers to plaintiffs on the premise that babies have suffered neurological impairment at birth. The purpose of this article is not to conduct scientific analysis but to discuss the knowledge currently available regarding cerebral palsy (CP), a neurological impairment that is among the more prevalent claims. This article instructs that if too little is known with a degree of probability sufficient to predict the outcomes, the physician cannot be responsible when the unfortunate outcome is cerebral palsy. Lawyers must learn how to defend these cases, and doctors must learn not to fear these cases. Furthermore, the defense bar must educate the court system with information sufficiently reliable to meet the scientific method, as against information that may indicate correlation but not causation. The bar also must emphasize evidence-based medicine over empirical-based medicine.

II.

The Origins of “Causation”

In the 1800's, an orthopedic surgeon named William Little proclaimed that children who developed cerebral palsy must have suffered problems during labor and delivery. Since that time, doctors and lawyers have consulted with each other to prove or disprove the substance of that claim. Sometime later, Sigmund Freud disputed Dr. Little’s claim by announcing that cerebral palsy was a problem contracted in utero. Many professionals likewise have held that mindset for a long time.[1] Under the circumstances, it is necessary to discuss some of the factors inherent in each of these premises. Historically, of course, it should be noted that many babies were born in homes or other non-hospital settings; only recently have hospitals, obstetricians, perinatologists, neonatologists, and neonatal units been available. Thus, for only a small period in history have obstetricians been available to deliver babies in hospitals. Furthermore, many children died at birth or shortly after birth because of a lack of medical care, and countries with insufficient medical care continue to suffer infant mortality. Of even greater concern is the topic of this article -- the instance of cerebral palsy in the live birth population. Since 1970, these statistics have increased, growing from 1.7 to 2.0 per 1,000 live births, to 2.0 to 2.5 per 1,000 live births.[2] Despite the better, more sophisticated standards of health care now available, the incidence of cerebral palsy has increased. This is decidedly not an expected trend.

III.

The Fetal Heart Monitor

In terms of attributing liability for a child with cerebral palsy to the health care provider, no single mechanical instrument has proved a greater factor than the fetal heart monitor (FHM). Much has been written about the fetal heart monitor, and this article makes no pretense about comprehensive coverage of that issue. The fetal heart monitor was developed in the late 1960's and was employed extensively in the early 1970's, becoming a standard measure of care from that time through to the present. Although much time and money was spent in developing the fetal heart monitor, essentially no money was spent in the final stages of development to test, record, study and prove the meaning of patterns as revealed by the tracings of a fetal heart monitor. This was clearly a fundamental mistake since much time has been spent since, debating the meaning of these tracings. Volumes of literature have been written on this topic. Even “experts” disagree on the various propositions. Most of the information, however, is merely hypothesis. At best, there are allegations which might be termed “correlations,” but information about the tracings discloses no causal relation to make them predictable of a fetal outcome.[3]

Under these circumstances, it is appropriate to discuss scientific method to some extent. Scientific method is a process of observation regarding some fact within the universe. The method is: (1) to observe some aspects of the universe; (2) to develop a hypothesis consistent with what has been observed; (3) to test the hypothesis in order to make predictions; (4) to test those predictions by experiments through further observations; and (5) to repeat steps 3 and 4 until there are no discrepancies between theory and experiment or observation.

When consistency is obtained, the hypothesis becomes a theory and provides a coherent set of propositions that explain a class of phenomena. A theory then operates as a framework within which observations are explained and predictions are made. The key to scientific methodology is to repeat certain steps until an outcome is predictable; that is, the outcome is not merely a factor or conjecture but a theory, such as the Theory of Gravity.

Within the context of scientific method, then, no fetal heart rate pattern can produce a predictable result; the results of tracings on fetal heart monitor strips simply cannot predict a fetal outcome. In particular, there is no pattern of tracing which dictates cerebral palsy. While there are alleged experts who are willing to testify, there are none who have a basis in scientific methodology to predict fetal outcome based on fetal heart rate tracings.

That being said, there does exist medical literature that would articulate how to interpret fetal heart monitor tracings, premised on the fact that these machines do exist. And since these machines exist, their usage has become common. As such, these machines have become relevant to the "standard of care." It is within that context that fetal heart monitors should be considered.

Since these machines are relevant to the standard of care, then, it is important to pursue another line of literature indicating the purpose of these machines. That is, what are these machines and what, in fact, do they show? There is no scientific method of proof indicating that fetal heart monitor tracings predict injury to a baby with any degree of certainty. Even more importantly, there is no proof that they predict an injury that produces cerebral palsy. Fetal heart monitor tracings are often termed "reassuring" or "non-reassuring," but they never are referred to as "predictive." In fact, approximately 95% of the time they were wrong. How then can the fetal heart monitor function as a vehicle for expert testimony in the courtroom? Obviously, this occurs only because courts have routinely allowed such testimony and because physicians are willing to testify that the fetal heart monitor affords some reliable and authoritative information.

In point of fact, the FHM machine communicates the heart rate of the fetus. It demonstrates whether the heart rate is up or down, whether it is developing a trend of being up or down, and its relationship to measured uterine contractions. In that regard the FHM machine can, in fact, be helpful, but it does not predict whether a child will develop cerebral palsy. Nor does it predict whether this particular bradycardia, for some period of time during the course of the labor, will cause that child to have cerebral palsy. Therefore, the predictability or diagnosis is not reliable. Under these circumstances, the defense bar must intensify its efforts to exclude the fetal heart monitor as a basis upon which to premise liability. This effort will involve more attention to detail, clearer knowledge about the monitor and its history of development, and a closer examination of the studies disclosing results of FHM usage.

IV.

Causes of Cerebral Palsy

The latest opinion published by the American College of Obstetrics and Gynecology suggests that the term "birth asphyxia" is persistently misused, with the misperception that it accounts for a significant portion of infants who are born with cerebral palsy. In point of fact, however, only severe and prolonged hypoxia is associated with an increased risk of subsequent neurologic dysfunction, but this level of hypoxia occurs only rarely, given the birthing conditions in the United States and modern industrialized countries.[4] Thus, the causes of cerebral palsy among infants remain largely unknown. In particular, there is no scientific method to prove that problems during labor and delivery are causative of cerebral palsy. One can make allegations that some extraordinary event occurs, such as significant trauma or other activity that may, in fact, be causative, but on a routine or reasonable basis, there is nothing upon which the leap to causation can be made.[5] In that regard, there are events that are clearly identifiable whose occurrence would require a physician to intervene immediately, such as placental abruption or a heart rate of fifteen to twenty beats per minute. However, these are not the situations discussed in this article.

The overall point is that many children have cerebral palsy and this medically sophisticated society simply doesn’t know why. What is known is that some children who were born after normal labor and delivery can have cerebral palsy. It is also known that children born after a very abnormal labor and delivery can have a normal outcome. Children are born with cerebral palsy who have experienced bradycardia, tachycardia, abnormal labor periods, prolonged labor, or any host of other scenarios that might occur during the course of labor and delivery. Were any of those events the cause of the cerebral palsy? Science cannot accurately translate to that conclusion. The fact of the matter is that every year many mothers or fetuses suffer these same complications, but the children are born without cerebral palsy. Therefore, there is nothing predictive about any particular event. Again, there may be correlation, but there is no evidence of causation, and no attempt to posit causation should be allowed to stand in the courtroom. Vigorous cross-examination and evidentiary development is necessary to show the difference between causation and correlation. Obtaining expert admissions about the history and the lack of testing/studies on FHM is the key to developing a strong case.

Cesarean Sections

In the 1980's, the prevalence of fetal heart monitors significantly influenced the cesarean section rate. In fact, litigation and fetal heart monitors impacted the cesarean rate, which climbed to as much as 33 to 35% of all pregnancies. At the hint of a late deceleration or perhaps after a late deceleration, bradycardia, or some other abnormality in the fetal heart monitor strip, the obstetrican would proceed with a cesarean section. Consequently, the number of cesarean sections skyrocketed, even though the mothers may have experienced only minimum events. However, it is now common knowledge that the skyrocketing number of cesarean sections did not improve the number of outcomes in relation to children with cerebral palsy, and the cesarean procedure places the mothers at a significant risk.

There is some notable disagreement about the rate of cerebral palsy. There are different quoted statistics, and one could argue that the numbers are better today than they were 30 years ago. One could even argue that neonatal units are keeping more preterm babies alive and, because more preterm babies are being kept alive, there is a higher rate of cerebral palsy. Thus, the rate goes up. There are probably modicums of truth contained in all these arguments. Nevertheless, the rate has increased. Fetal heart monitors have not caused the incidence of cerebral palsy to decrease, the increase in cesarean sections did not cause a decrease in the rate of cerebral palsy, nor did any other intervention or activity that obstetricians have employed. Logically, then, obstetrical interventions have had no impact on the cerebral palsy development; they don’t prevent it, nor do they cause it. Furthermore, it is important to note that despite enhanced prenatal care, including better nutrition, more frequent monitoring and more attention to labor and deliveries, the incidence of cerebral palsy has gone up, not down.

Thus, when discussing the causes of cerebral palsy, what is known is that science knows nothing, and if science knows nothing, how can experts testify to probabilities? How can an expert claim that cerebral palsy is predictable? Of course, there are many things in nature that are unknown, beyond these issues in medicine. With sophisticated computer systems and years of historical information, even the weather cannot be predicted with any degree of certainty. It can be discussed after the fact, but not before. Thus, it should come as no surprise that a baby’s outcome cannot be predicted. The problem is that nowhere else in nature are millions of dollars transferred from one side of the table to another when there is no degree of predicting cause.

VI.

Other Matters of Diagnosis

Frankly, over the last twenty-five years, numerous attempts have been made to clarify and diagnose when some event has occurred to produce a hypoxic ischemic event, or when some incident occurred that caused cerebral palsy. To date, science has been unable to produce a reliable degree of probability allowing the cause of cerebral palsy to be predicted with any certainty. Discussion of some examples is in order.

A. Meconium Staining

In the late 1970's and early 1980's, many obstetricians and pediatricians or pediatric neurologists held the view that meconium staining, evident at the time of birth, clearly indicated that the baby had suffered stress in utero. Such staining would also indicate that the stress was significant enough to produce some kind of brain damage, making the child identifiable as a cerebral palsy child.[6] Further study, evaluation and retroactive studies have clearly indicated that this is not the case. Many babies have meconium staining at birth and do not have a diagnosis of cerebral palsy. In fact, many more have meconium staining who never have cerebral palsy, and certainly cerebral palsy occurs without meconium staining. Therefore, meconium staining is not predictive. There is no degree of probability associated with such staining, much less anything that meets the ordinary scientific method.[7]

B. Nucleated Red Blood Cell

Likewise, in the late 1980's and early 1990's several physicians studied the topic of nucleated red blood cells. It was determined that if physicians could identify the number of nucleated red blood cells in the blood shortly after birth, this would provide some sense of whether or not an event had occurred that would require repair, i.e., an increased number of nucleated red blood cells. This phenomenon would demonstrate that the body was trying to develop cells to repair some damage that had occurred to the system. Therefore, physicians could work backwards to identify where the curve occurred in the production of nucleated red blood cell numbers and establish whether the injury had been sustained a day ago, a week ago or months ago. This theory still exits today, but it is continually under study and is not finalized. It is of no help in predicting a child’s outcome or predicting exactly what injury occurred. Furthermore, it is after the fact.[8]

C. Neuroradiology

In the late 1980's, with the advent of CT scans, MRI’s, and ultrasound technology, it was prophesied that the timing of hypoxic ischemic injuries would be very obtainable. This information coincided with the advent of clinical signs such as bulging fontanels and head circumferences, as well as other clinical factors. The CT scans, the MRI’s, and ultrasounds will, of course, indicate subarachnoid hemorrhages, subdural hematomas and caputs. Even more important, perhaps, these tools will show ventricle sizes. Small ventricles indicate swelling, whereas large ventricles indicate lack of development.

While these tests are important, however, they are not finalized; different methodologies and further studies are necessary. Even more significant, there is no way to test the hypothesis. One can examine a ventricle and say, “This swelling has to be two weeks old,” but how does one know? The development of brain swelling from a hypoxic ischemic event does not normally produce this finding. Certainly brain structure is visible, but its deficits cannot be clearly timed to development or injury.[9]

D. Infantile Spasms/Seizure Activity

In the late 1970's it was clearly believed that the timing of a newborn’s spastic activity was indicative of when a hypoxic ischemic event had occurred and whether the event was related to labor and delivery or to some other in utero occurrence. Usually, the infantile spasms would occur within twelve to twenty-four hours or twelve to thirty-six hours from birth. If they occurred earlier than that, they were not related to labor and delivery; if they occurred later than that, they represented a developmental or genetic issue. This is not recognized methodology for making such diagnoses today. Further, many neonates have seizure activity but never develop cerebral palsy. Thus, once again, these events are non-predictive of a particular outcome. If seizure activity is not predictive of outcome, nor of the timing of an in utero event, why would it serve as a foundation for opinions about when a child developed cerebral palsy?[10]

E. Placenta

Perhaps one of the newer and more rapidly developing areas of study has involved the placenta. When preserved following delivery, the placenta is an organ that can be sectioned and studied. In that regard, it is similar to the rings of a tree. It may provide historical information about the progress of this fetus in utero and offer some firm understanding as to what has occurred. The development of this science is not universal at this time, however, nor do pathologists agree about all of the findings. The study represents a continuing developmental process. Once again, it is not definitive. Besides, the placenta cannot be studied until after the fact. Thus, even if routine agreement existed about some particular finding and its relation to cerebral palsy, a study would be required of all similar children to connect the finding with some other event in order to identify the agent causing cerebral palsy. Again, the placenta may prove helpful regarding diagnosis and causation, but it cannot be used until the child is born.[11]

F. Systemic Injuries

Another predominant theory concerned systemic injuries. This theory maintained that an hypoxic ischemic encephalopathy event would produce a number of systemic injuries before damage to the brain would occur. Damage to the cardiovascular system, the intestinal tract, the renal system and others occurs before the lack of oxygenation impacts the brain. This theory itself was based on the diving reflex that caused oxygen-carrying blood to shunt to the brain, diverting it from the rest of the body. However, this theory now has undergone some reconsideration. It was significant to the defense to show that there could be no hypoxic ischemic injury during labor and delivery because the other body systems functioned within the normal range. Particularly helpful was the renal system, showing normal urination pattern subsequent to birth, as well as a normal BUN or creatinine level. From this data, the defense could advance that there had been no hypoxic ischemic event. While this still is a rational approach, there is now some controversy since the diving reflex is no longer recognized. Stated another way, brain damage can occur even though other bodily systems may not suffer from hypoxic ischemic injury.[12]

G. The Old Standbys

Apgar scores were initially thought to be predictive of whether a child ultimately would be diagnosed with cerebral palsy. No longer is that the case. It is always better to have good Apgar scores because that means the child is doing well after delivery. However, bad Apgar scores at five and ten minutes do not predict that the child will develop cerebral palsy later in life. Furthermore, an infant’s blood gases at time of birth, when showing below a pH of 7.0, were thought to portray a significant level of acidosis. Although this level is still recognized as demonstrating a significant level of acidosis, it is not predictive of the child’s outcome. In short, central nervous system deficits are not predictable from this evidence, not to mention the fact that it is difficult, if not impossible, to obtain blood gas studies before delivery. Equally non-predictive is the effort to tie low blood gases to some event occurring during the course of labor and delivery which will establish a clinical sign that a baby will have low blood gas scores. Once again, they are not predictive of outcome.

H. Genetics

In the field of medicine, daily strides are made regarding genetic discovery. Currently, however, this field of study is not concluded. As it may relate to cerebral palsy at least, I have often heard trial experts describe the study of genetics in these words: “We can study a line of pick-up trucks loaded with tomatoes, but we cannot study the tomatoes, and the tomatoes are the keys.” There are an enormous number of unknowns. In particular, there is no gene identified as the cause for cerebral palsy for which science can test. Of course, there exist other identified genes whose presence will predict certain factors that are always present with certain diseases. It is equally likely that genetics may be the sole cause of cerebral palsy, or at least the prevailing cause. Genetics controls most other factors in human life. In the course of the past twenty years, many syndromes have been developed or discovered that may relate to cerebral palsy, but once again, these are not predictive of the outcome of the neonate.

VII.

How to Develop the Truth

It would seem that the development of this material for the purpose of fair and reasonable presentation to a trier of facts, or a review board, or a peer review process must include some of the following factors. First, there is the matter of educating a tribunal with experts and literature, and developing experts who hold a realistic awareness of the scope of information available in medical libraries. Experts must be prepared to inform these tribunals about the parameters of existing studies.

If scientific methodology were applied, many opinions regarding the cause of cerebral palsy would be disallowed in a carefully scrutinized setting. The courtroom is not a place for guessing. Opinions must be based upon known facts and recognized scientific information. This is a difficult area, but the courts have become more wary of opinions that are not premised on scientific information. Courts have developed methods of scrutinizing expert opinions before they are conveyed to the jury. Every effort to utilize scientific information should be followed. Even if inaccurate information becomes a matter of evidence, defense counsel should use the opportunity to identify discrepancies in theory or thought process.

It is also important to concentrate on these facts:

· No fetal heart monitor tracing is predictive for cerebral palsy; in fact, cerebral palsy is not predictable by any fact or factors.

· No meconium staining, no heart rate tracing, no hemorrhaging, no hematomas, no Apgar score and no acidosis level will predict cerebral palsy.

· No labor pattern or time of labor will predict the occurrence of cerebral palsy.

· Numerous theories have come and gone; some have resurfaced over time without any predictable results.

· There is overwhelming medical literature about the causation (or lack of same) for cerebral palsy from any set of medical facts.

From all the foregoing analysis, there still exists one overriding question: "If the cause or causes of cerebral palsy remain unknown, why should doctors or health care providers still be liable?" In this regard, the standard of care must be addressed particularly.

Although enormous quantities of information regarding standard of care are involved, it should be noted that these standard of care issues do not relate to cerebral palsy causation. The standard of care regarding whether certain things are done or not done during the course of labor and delivery may well apply to other issues, but it does not apply to cerebral palsy. This fact must be emphasized because the standard of care was never designed or determined for the sole purpose of preventing cerebral palsy. Since cerebral palsy cannot be predicted, how could a standard of care be directed to that subject?

Experts must be challenged continuously on the topics noted in this article and their knowledge of the studies involved. That which is known versus that which is not could make all the difference for successful defense.

VIII.

Conclusion

What is known about cerebral palsy and its causation is simply that nothing is known. No scientific or medical studies reasonably predict what will occur with any particular fetus prior to the time of its delivery. What’s more, no methodology exists to test any given premise. That is particularly true with cerebral palsy. Oftentimes, however, parents are unwilling to accept that the problem might be genetic or that the problem simply might be unexplainable. Parents would rather locate some defined cause, and that cause too often becomes the physician or health care provider. The fact finder must be given to understand that the physician and the health care provider have become convenient targets for scientific uncertainty.

Bibliography

1. A. James Barkovich & Charles L. Truwit, Brain Damage from Perinatal Asphyxia: Correlation of MR Findings with Gestational Age, 11 AJNR 1087-96 (Nov./Dec. 1990).

2. Frank H. Boehm, Intrapartum Fetal Heart Rate Monitoring, 26 Obstetrics and Gynecology Clinics of North America 623-39 (Dec. 1999).

3. Robert L Bryce et al., Association Between Indicators of Perinatal Asphyxia and Adverse Outcome in the Term Infant: A Methodological Review, 4 Neuroepidemiology 24-38 (1985).

4. Committee Opinion, Utility of Umbilical Cord Blood Acid-Based Assessment, American College of Obstetrics and Gynecology, No. 138, Apr. 1994.

5. A. Emond et al., Cerebral Palsy in Two National Cohort Studies”, 64 Archives of Disease in Childhood 848-52 (1989).

6. John M. Freeman & Karin Nelson, Intrapartum Asphyxia and Cerebral Palsy, 82 Pediatrics No. 2, at 240-49 (August 1988).

7. G. Gaffney et al., Case-Control Study of Intrapartum Care, Cerebral Palsy, and Perinatal Death”, 308 British Medical Journal 743-50 (Mar. 19, 1994).

8. Jin S. Hahn, Correlation of Clinical Finding and Timing of the Asphyxial Event, Ch. 21 at 356-73 in Fetal and Neonatal Brain Injury (David K. Stevenson & Philip Sunshine eds., 2d ed. 1997).

9. Kathleen M. Hanlon-Lundberg et al., Nucleated Red Blood Cells in Cord Blood of Singleton Term Neonates, 176 American Journal of Obstetrics & Gynecology 1149-56 (June 1997).

10. Cynthia Kaplan et al., College of American Pathologists Conference XIX on the Examination of the Placenta: Report of the Working Group on the Definition of Structural Changes Associated with Abnormal Function in the Maternal/Fetal/Placenta Unit in the Second and Third Trimesters, 115 Arch. Pathol. Lab. Med. 709-16 (July 1991).

11. Lisa M. Korst et al., Nucleated Red Blood Cells: An Update on the Marker for Fetal Asphyxia, American Journal of Obstetrics & Gynecology 841-46 (Oct. 1996).

12. K.C.K. Kuban & Alan Leviton, Cerebral Palsy, 330 New England Journal of Medicine 188-95 (January 20, 1994).

13. Claire Langston et al., Practice Guideline for Examination of the Placenta, 121 Arch Pathol Lab Med 449-76 (May 1997).

14. Enid Leikin et al., Relationship Between Neonatal Nucleated Red Blood Cells Counts and Hypoxia-Ischemia Injury, 87 Obstetrics & Gynecology 439-43 (Mar. 1996).

15. Paul J. Melone et al. Appropriateness of Intrapartum Fetal Heart Rate Management and Risk of Cerebral Palsy, 165 American Journal of Obstetrics Gynecology 272-77 (Aug. 1991).

16. Karin B. Nelson & Jonas H. Ellenberg, Antecedents of Cerebral Palsy, 315 New England Journal of Medicine 81-86 (July 10, 1986).

17. Karin B. Nelson & Jonas H. Ellenberg, Antecedents of Seizure Disorders in Early Childhood, 140 American Journal of Diseases of Children 1053-61 (Oct. 1986).

18. Karin B. Nelson et al., Uncertain Value of Electronic Fetal Monitoring in Predicting Cerebral Palsy, 334 New England Journal of Medicine 613-18 (Mar. 7, 1996).

19. Nigel Paneth, Birth and the Origins of Cerebral Palsy, 315 New England Journal of Medicine 124-26 (July 10, 1986).

20. Nigel Paneth, Etiologic Factors in Cerebral Palsy, 15 Pediatric Annuals 191-201 (March 1986).

21. Jeffrey P. Phelan et al., Intrapartum Fetal Asphyxial Brain Injury with Absent Multiorgan System Dysfunction, 7 Journal of Maternal-Fetal Medicine 19-22 (1998).

22. Jeffrey P. Phelan et al., Neonatal Nucleated Red Blood Cell and Lymphocyte Counts in Fetal Brain Injury, 91 Obstetrics & Gynecology 485-89 (Apr. 1998).

23. Jeffrey P. Phelan et al., Nucleated Red Blood Cells: A Marker for Fetal Asphyxia?, 173 American Journal of Obstetrics Gynecology 1380-84 (Nov. 1995).

24. Mortimer G. Rosen & Janet C. Dickinson The Incidence of Cerebral Palsy, 167 American Journal of Obstetrics & Gynecology 417-23 (Aug. 1992).

25. Judy V. Schmidt & Robin McCartney, History and Development of Fetal Heart Assessment: A Composite, 29 JOGNN 295-305 (May/June 2000).

26. Fiona J. Stanley & Linda Watson Trends in Perinatal Mortality and Cerebral Palsy in Western Australia, 304 British Medical Journal 1658-63 (1992).

27. Joseph J. Volpe, Neurology of the Newborn (4th ed. 2001).

28. Thomas E. Wiswell, Meconium Staining and the Meconium Aspiration Syndrome, Ch. 32 at 539-63 in Fetal and Neonatal Brain Injury (David K. Stevenson & Philip Sunshine eds., 2d ed. 1997).

How to Develop the Truth

Conclusion

ENDNOTES