MEDICAL LITERATURE & CAUSATION IN CEREBRAL PALSY CASES
This article will address the issue of causation in cerebral palsy cases. It includes a review of the pertinent medical literature dealing with the relationship between birth trauma and cerebral palsy. Included in such literature are publications by the American College of Obstetricians and Gynecologists (ACOG), which purport to establish required medical findings as a prerequisite to associating perinatal (pertaining to the time and process of giving birth or being born) events with cerebral palsy. Finally, it will review recent cases which have held that the aforementioned ACOG literature is not generally accepted in the medical community.
The leading text on pediatric neurology (Volpe) contains the following reprint of an exchange of viewpoints published in The Lancet :
EDITORIAL – ANONYMOUS – NOVEMBER 25, 1989
In light of the evidence reviewed above, the continued willingness of doctors to reinforce the fable that intrapartum care is an important determinant of cerebral palsy can only be regarded as shooting the specialty of obstetrics in the foot.
LETTER TO THE LANCET:
However medicolegally comforting the new epidemiological orthodoxy you espouse may be, most of us will continue to believe that severe hypoxia/ischemia is deleterious to the brain, that the longer it goes on the worse the effect, and that delayed, inefficient, or inappropriate treatment can be disastrous. It is no longer a matter for conjecture whether asphyxia and cerebral damage are causally related, or merely occur in the same antenatally imperfect individual. Ultrasonography, and many other objective tests of cerebral structure and function allow us to follow the time course of evolving neuronal damage in the postnatal period following severe asphyxia.
You suggest that by accepting “...the fable that intrapartum care is an important determinant of cerebral palsy,” the specialty of obstetrics is shooting itself in the foot, and that it is time to look elsewhere. We are concerned that by ignoring the 23% of cerebral palsy that is related to intrapartum asphyxia, obstetricians and their colleagues will take the advice too literally and shoot themselves somewhere else.
Causation - A Plaintiff’s Burden
RSA 507-e:2 (Burden of Proof) requires that a plaintiff in a medical malpractice case prove by affirmative evidence, including expert testimony, that the medical care provider failed to act in accordance with the “standard of reasonable professional practice” and “( c ) That as a proximate result thereof, the injured person suffered injuries which would not otherwise have occurred.” (Emphasis added). Proof of causation in medical malpractice cases is not dissimilar to the general common law duty in tort actions, to causally relate the underlying negligence to the resulting injury. Causation has become an especially fierce battleground in medical negligence law.
Ordinarily, a plaintiff in such cases will address his or her burden on the issue of causation through both expert testimony, and medical literature – admitted into evidence pursuant to Rule 803 (18), which states:
(18) Learned Treatise
To the extent called to the attention of an expert witness upon cross-examination or relied upon by the witness in direct examination, statements contained in published treatises, periodicals, or pamphlets on a subject of history, medicine, or other science or art, established as a reliable authority by the testimony or admission of the witness or by other expert testimony or by judicial notice. If admitted, the statements may be read into evidence, but may not be received as exhibits unless the Court finds that the probative value of the statements outweigh their prejudicial effect.
The rationale for this exception to the hearsay rule was that learned treatises, including medical literature, had adequate assurances of trustworthiness to allow for their use without providing for the usual safeguard of cross-examination of the declarant. Those assurances were thought to be a lack of bias, a desire to accurately state the truth (including the author’s knowledge that peer review is likely), and an author’s motivation to safeguard his or her reputation.
Definitions
Addressing the issue of whether there is a causal link between cerebral palsy and birth trauma requires an understanding of some of the pertinent medical terminology:
Asphyxia is the state in which pulmonary or placental gas exchange is disrupted leading to decreased oxygen and increased carbon dioxide in the blood and tissues.
Hypoxia is the reduction of oxygen to body tissue.
Hypoxemia is the reduction of oxygen in the blood stream.
Ischemia is a reduction in or cessation of blood flow to tissues, including the brain.
Acidemia is the increased concentration of hydrogen in the blood.
Hypoxic ischemic encephalopathy (HIE) is a type of neurologic injury to a newborn in which the etiology is considered to be a reduced oxygen or blood flow at or near the time of birth.
Cerebral palsy is a static, non-progressive motor impairment of early onset that is cerebral in origin with multiple possible causes.
Apgar score is the evaluation of an infant’s physical condition, usually performed 1 minute and again 5 minutes after birth, based on a rating of five factors that reflect the infant’s ability to adjust to extrauterine life.
Acidosis is an abnormal increase in hydrogen ion concentration in the body, resulting from an accumulation of an acid or the loss of a base.
Questionable Literature
The assurances of trustworthiness underlying the exception to the hearsay rule contained in Rule 803 (18) have been brought into question. One critical review of Rule 803 (18)’s permissive use of medical literature as evidence, concluded that the underlying research was unregulated, subject to falsification, frequently of poor quality, and often “dubious.” The authors of another review concluded that “litigation science” had invaded the realm of scientific research in order to attempt to influence litigation. Medical research and literature on the specific issue of causation of cerebral palsy has also been questioned.
In 1992, the American College of Obstetricians and Gynecologists (ACOG) published Technical Bulletin No. 163 which has since been withdrawn. Technical Bulletin No. 163 was not authored, but lists Karin Nelson, M.D. as a source in 7 of its 28 footnotes and thanks her for her assistance in development of the bulletin. Bulletin 163 purported to establish “essential criteria” before a plausible link can be made between cerebral palsy and events occurring during labor and delivery. Dr. Nelson has been quoted as saying that these criteria were “intended for litigation.” Those criteria were stated to be:
1. Profound umbilical artery acidemia (pH < 7.00).
2. Apgar score of 0-3 for > 5 minutes.
3. Neonatal neurologic sequela, e.g. seizures, coma, hypotonia.
4. Multi-organ system dysfunction.
These same criteria have been incorporated into the January 2003 ACOG and American Academy of Pediatrics (AAP) publication -- Neonatal Encephalopathy and Cerebral Palsy (NEACP), as well as several medical
texts.
ACOG has been unable to remain objective when addressing the issue of causation of cerebral palsy, and in medical malpractice generally. In a submission to the House of Representatives Subcommittee on Health, dated February 27, 2003, ACOG argues at length for curbs on “excessive litigation,” and asserts that we live in a “lawsuit culture where doctors are held responsible for less than perfect outcomes.” It has also described the medical malpractice problem as being caused by the perception that obstetricians are “deep pockets for claims based upon a variety of untoward outcomes associated with the human condition.” ACOG spends substantial sums on lobbying such positions. This self-interest and lack of objectivity leads to a legitimate suspicion of the reliability of ACOG’s research and publications on this issue.
Reason to Question the “Essential” Criteria
The “essential” criterion of an Apgar score of no more than 3 for more than 5 minutes appears to have little support in the literature. It has not held up to scrutiny and it is neither sensitive nor specific in predicting cerebral palsy. In one study of 47 infants who had suffered intrapartum asphyxia, only 26 (55%) of them had Apgar scores of 3 or less at 5 minutes. One authority has expressed the opinion that a score of 6 or less at 5 minutes is more appropriate for providing a link between intrapartum asphyxia and the status of the infant at birth.
There is also a lack of consensus regarding at least one other “essential” criterion; namely, the level of acidosis necessary to make an association between cerebral palsy and birth injury. The level of acidosis has been variously placed at pH < 7.20; 7.10, or < 7.00. In fact, when looking at all 4 “essential criteria” for the 47 infants in the previously cited study, only 10 (21%) met all of them; thus, the authors concluded that ACOG Technical Bulletin No. 163 was not valid as an acute intrapartum asphyxial model. A similar conclusion was reached in another study of 351 full-term infants suffering from neonatal encephalopathy, seizures, or both.
Literature Supporting Causation
As the author of the letter to The Lancet expressed, there is obvious reason for the belief that a severe reduction in oxygen or blood flow to a fetus, at around the time of birth is harmful to the fetus’s brain. Animal studies support that conclusion.
A study of primate fetuses which had been cruelly (by today’s standards) subjected to acute and total asphyxia (total umbilical cord occlusion) was published in 1963. Those primate fetuses which had been subjected to asphyxia for less than 6 minutes were neurologically normal; those subjected to between 7 to 9 minutes of asphyxia sustained varying degrees of neurologic damage, but behaved normally; and those subjected to 15 or 16 minutes of asphyxia suffered severe neurological deficits with symptoms closely resembling cerebral palsy. Another study from 1972 described in excruciating detail, the means by which total asphyxia was achieved in its experimental subjects and the struggles of those infant monkeys to breathe. That study reported similar findings regarding neurological injury to the asphyxiated subjects and described the pattern of injuries, including the
relationship to the degree of asphyxia.
Although there may be many causes of fetal brain damage which lead to cerebral palsy, it should be beyond dispute that asphyxia is one of them. In Fetal Medicine Principles and Practice, the author reasons:
There is no doubt that asphyxia, if of sufficient severity and duration, can cause irreversible neuronal damage in the extrauterine patient, and no reason to doubt that the same effect could and does occur in the intrauterine patient, the fetus.
In Neurology of the Newborn, Dr. Volpe estimates that 12% to 23% of cerebral palsy is related to intrapartum asphyxia. Others give higher estimates. One study of 40 infants with documented seizures of various etiologies found that asphyxia was the most common cause of acute encephalopathy. Another authority on the subject has concluded that intrapartum asphyxia is a “major cause of acute mortality and chronic neurological disability in survivors.” He also noted that distinguishing infants suffering from intrapartum asphyxia from those with congenital diseases is relatively easy. The consequence of such morbidity is not insignificant; as stated by Dr. Volpe:
In view of the relatively high prevalence of cerebral palsy in most countries, generally 2 to 3 cases per 1,000 children born, even a relatively small percentage of cases caused by intrapartum events translates into a very large absolute number.
An interesting finding from one pertinent study was that infants born at night were more than twice as likely to die from asphyxia than those born during the day. The authors attributed that finding to “tiredness and inexperience of the night time staff, or a delay in appropriate treatment.” That same study found evidence from “confidential inquiries” into neonatal encephalopathy and deaths of term infants, that there had been a high proportion of “less than optimum care” during labor.
Relevant Cases
In the recent and important case of Tavares v. New York City Health and Hospitals Corporation, the defense sought a pretrial exclusion of the plaintiff’s experts’ opinions, characterizing them as medically unsound. Specifically, the defendants alleged that the plaintiff’s experts’ failure to adhere to the 4 “essential criteria” of Technical Bulletin 163 demonstrated a lack of general acceptance of such opinions. The Court made a detailed review of the pertinent medical literature, including the history behind Technical Bulletin 163 and NEACP, denied the defendants’ motion, and concluded:
...the theories advanced...that a rigid criteria of three or four factors must be present to find that cerebral palsy was caused by asphyxia or by a hypoxic event, are not generally accepted by the medical community as necessary to a diagnosis of neurological defect. Rather, plaintiffs have demonstrated that many authorities have indicated that the Apgar score and pH level are poor indicators of neurological defects and that not all infants born suffering from cerebral palsy have multiorgan involvement.
Further, the literature cited also demonstrates that Bulletin 163, the BMJ Template, and Chapter 8 have been criticized for lack of reliability. Based upon this analysis, it is determined that defendant has failed to establish that the theory relied upon by plaintiffs’ expert is novel and not generally accepted in the medical community, as is required by the Frye standard if the testimony is to be precluded....
Another important case on this issue is 1st Of America Bank v. USA. In a bench trial, the judge faced a similar challenge to the one presented to the court in Tavares, supra. The opinion testimony of several defense witnesses regarding causation had changed because of self-described “evolution” of their thinking. These defense experts initially attributed the minor plaintiff’s neurologic injuries to severe perinatal asphyxia; however, by the time of trial they had concluded that the cause of neurologic injury was unknown, but could not have been caused by perinatal asphyxia. That change in opinion was largely based upon the witnesses’ reading of the literature published by Karin Nelson, M.D. and Bulletin 163. The court found the reasoning behind the “evolution” of opinion suspect, as well as the underlying research which allegedly prompted the change in testimony, and ruled:
The Court finds these criteria of questionable value in litigation. If a court held a plaintiff to these criteria before finding causation as a result of perinatal asphyxia, plaintiff would be required to do more than demonstrate causation by a preponderance of the evidence. Plaintiff’s proof would have to be essentially conclusive.
Regarding the admissibility of questionable medical literature, generally, the case of O’Brien v. Angley , is instructive. The defense offered in evidence a portion of an editorial from the Journal of American Medical Association (JAMA). The trial court permitted its introduction as an exception to the hearsay rule pursuant to Rule 803 (18). The Ohio Supreme Court reversed holding that the editorial was primarily an expression of opinion on a controversial subject and was not a legitimate “learned treatise.” The Court held that where an:
author publishes an article with a view toward litigation, or where he possesses a personal interest in a litigable matter, a probability of bias exists which undermines the logic supporting the admission of this material in evidence as an exception to the rule against hearsay.
Conclusion
An objective review of the medical literature on the causes of cerebral palsy demonstrates that ACOG’s “essential criteria” are unreliable and not generally accepted in the medical community. Counsel should be alert to the need to challenge efforts to portray such literature as setting the standard for causation in birth injury cerebral palsy cases.
Reis Law, PLLC
66 Hanover St. Suite 203
Manchester, NH 03101
Ph: 603-792-0800
This article will address the issue of causation in cerebral palsy cases. It includes a review of the pertinent medical literature dealing with the relationship between birth trauma and cerebral palsy. Included in such literature are publications by the American College of Obstetricians and Gynecologists (ACOG), which purport to establish required medical findings as a prerequisite to associating perinatal (pertaining to the time and process of giving birth or being born) events with cerebral palsy. Finally, it will review recent cases which have held that the aforementioned ACOG literature is not generally accepted in the medical community.
The leading text on pediatric neurology (Volpe) contains the following reprint of an exchange of viewpoints published in The Lancet :
EDITORIAL – ANONYMOUS – NOVEMBER 25, 1989
In light of the evidence reviewed above, the continued willingness of doctors to reinforce the fable that intrapartum care is an important determinant of cerebral palsy can only be regarded as shooting the specialty of obstetrics in the foot.
LETTER TO THE LANCET:
However medicolegally comforting the new epidemiological orthodoxy you espouse may be, most of us will continue to believe that severe hypoxia/ischemia is deleterious to the brain, that the longer it goes on the worse the effect, and that delayed, inefficient, or inappropriate treatment can be disastrous. It is no longer a matter for conjecture whether asphyxia and cerebral damage are causally related, or merely occur in the same antenatally imperfect individual. Ultrasonography, and many other objective tests of cerebral structure and function allow us to follow the time course of evolving neuronal damage in the postnatal period following severe asphyxia.
You suggest that by accepting “...the fable that intrapartum care is an important determinant of cerebral palsy,” the specialty of obstetrics is shooting itself in the foot, and that it is time to look elsewhere. We are concerned that by ignoring the 23% of cerebral palsy that is related to intrapartum asphyxia, obstetricians and their colleagues will take the advice too literally and shoot themselves somewhere else.
Causation - A Plaintiff’s Burden
RSA 507-e:2 (Burden of Proof) requires that a plaintiff in a medical malpractice case prove by affirmative evidence, including expert testimony, that the medical care provider failed to act in accordance with the “standard of reasonable professional practice” and “( c ) That as a proximate result thereof, the injured person suffered injuries which would not otherwise have occurred.” (Emphasis added). Proof of causation in medical malpractice cases is not dissimilar to the general common law duty in tort actions, to causally relate the underlying negligence to the resulting injury. Causation has become an especially fierce battleground in medical negligence law.
Ordinarily, a plaintiff in such cases will address his or her burden on the issue of causation through both expert testimony, and medical literature – admitted into evidence pursuant to Rule 803 (18), which states:
(18) Learned Treatise
To the extent called to the attention of an expert witness upon cross-examination or relied upon by the witness in direct examination, statements contained in published treatises, periodicals, or pamphlets on a subject of history, medicine, or other science or art, established as a reliable authority by the testimony or admission of the witness or by other expert testimony or by judicial notice. If admitted, the statements may be read into evidence, but may not be received as exhibits unless the Court finds that the probative value of the statements outweigh their prejudicial effect.
The rationale for this exception to the hearsay rule was that learned treatises, including medical literature, had adequate assurances of trustworthiness to allow for their use without providing for the usual safeguard of cross-examination of the declarant. Those assurances were thought to be a lack of bias, a desire to accurately state the truth (including the author’s knowledge that peer review is likely), and an author’s motivation to safeguard his or her reputation.
Definitions
Addressing the issue of whether there is a causal link between cerebral palsy and birth trauma requires an understanding of some of the pertinent medical terminology:
Asphyxia is the state in which pulmonary or placental gas exchange is disrupted leading to decreased oxygen and increased carbon dioxide in the blood and tissues.
Hypoxia is the reduction of oxygen to body tissue.
Hypoxemia is the reduction of oxygen in the blood stream.
Ischemia is a reduction in or cessation of blood flow to tissues, including the brain.
Acidemia is the increased concentration of hydrogen in the blood.
Hypoxic ischemic encephalopathy (HIE) is a type of neurologic injury to a newborn in which the etiology is considered to be a reduced oxygen or blood flow at or near the time of birth.
Cerebral palsy is a static, non-progressive motor impairment of early onset that is cerebral in origin with multiple possible causes.
Apgar score is the evaluation of an infant’s physical condition, usually performed 1 minute and again 5 minutes after birth, based on a rating of five factors that reflect the infant’s ability to adjust to extrauterine life.
Acidosis is an abnormal increase in hydrogen ion concentration in the body, resulting from an accumulation of an acid or the loss of a base.
Questionable Literature
The assurances of trustworthiness underlying the exception to the hearsay rule contained in Rule 803 (18) have been brought into question. One critical review of Rule 803 (18)’s permissive use of medical literature as evidence, concluded that the underlying research was unregulated, subject to falsification, frequently of poor quality, and often “dubious.” The authors of another review concluded that “litigation science” had invaded the realm of scientific research in order to attempt to influence litigation. Medical research and literature on the specific issue of causation of cerebral palsy has also been questioned.
In 1992, the American College of Obstetricians and Gynecologists (ACOG) published Technical Bulletin No. 163 which has since been withdrawn. Technical Bulletin No. 163 was not authored, but lists Karin Nelson, M.D. as a source in 7 of its 28 footnotes and thanks her for her assistance in development of the bulletin. Bulletin 163 purported to establish “essential criteria” before a plausible link can be made between cerebral palsy and events occurring during labor and delivery. Dr. Nelson has been quoted as saying that these criteria were “intended for litigation.” Those criteria were stated to be:
1. Profound umbilical artery acidemia (pH < 7.00).
2. Apgar score of 0-3 for > 5 minutes.
3. Neonatal neurologic sequela, e.g. seizures, coma, hypotonia.
4. Multi-organ system dysfunction.
These same criteria have been incorporated into the January 2003 ACOG and American Academy of Pediatrics (AAP) publication -- Neonatal Encephalopathy and Cerebral Palsy (NEACP), as well as several medical
texts.
ACOG has been unable to remain objective when addressing the issue of causation of cerebral palsy, and in medical malpractice generally. In a submission to the House of Representatives Subcommittee on Health, dated February 27, 2003, ACOG argues at length for curbs on “excessive litigation,” and asserts that we live in a “lawsuit culture where doctors are held responsible for less than perfect outcomes.” It has also described the medical malpractice problem as being caused by the perception that obstetricians are “deep pockets for claims based upon a variety of untoward outcomes associated with the human condition.” ACOG spends substantial sums on lobbying such positions. This self-interest and lack of objectivity leads to a legitimate suspicion of the reliability of ACOG’s research and publications on this issue.
Reason to Question the “Essential” Criteria
The “essential” criterion of an Apgar score of no more than 3 for more than 5 minutes appears to have little support in the literature. It has not held up to scrutiny and it is neither sensitive nor specific in predicting cerebral palsy. In one study of 47 infants who had suffered intrapartum asphyxia, only 26 (55%) of them had Apgar scores of 3 or less at 5 minutes. One authority has expressed the opinion that a score of 6 or less at 5 minutes is more appropriate for providing a link between intrapartum asphyxia and the status of the infant at birth.
There is also a lack of consensus regarding at least one other “essential” criterion; namely, the level of acidosis necessary to make an association between cerebral palsy and birth injury. The level of acidosis has been variously placed at pH < 7.20; 7.10, or < 7.00. In fact, when looking at all 4 “essential criteria” for the 47 infants in the previously cited study, only 10 (21%) met all of them; thus, the authors concluded that ACOG Technical Bulletin No. 163 was not valid as an acute intrapartum asphyxial model. A similar conclusion was reached in another study of 351 full-term infants suffering from neonatal encephalopathy, seizures, or both.
Literature Supporting Causation
As the author of the letter to The Lancet expressed, there is obvious reason for the belief that a severe reduction in oxygen or blood flow to a fetus, at around the time of birth is harmful to the fetus’s brain. Animal studies support that conclusion.
A study of primate fetuses which had been cruelly (by today’s standards) subjected to acute and total asphyxia (total umbilical cord occlusion) was published in 1963. Those primate fetuses which had been subjected to asphyxia for less than 6 minutes were neurologically normal; those subjected to between 7 to 9 minutes of asphyxia sustained varying degrees of neurologic damage, but behaved normally; and those subjected to 15 or 16 minutes of asphyxia suffered severe neurological deficits with symptoms closely resembling cerebral palsy. Another study from 1972 described in excruciating detail, the means by which total asphyxia was achieved in its experimental subjects and the struggles of those infant monkeys to breathe. That study reported similar findings regarding neurological injury to the asphyxiated subjects and described the pattern of injuries, including the
relationship to the degree of asphyxia.
Although there may be many causes of fetal brain damage which lead to cerebral palsy, it should be beyond dispute that asphyxia is one of them. In Fetal Medicine Principles and Practice, the author reasons:
There is no doubt that asphyxia, if of sufficient severity and duration, can cause irreversible neuronal damage in the extrauterine patient, and no reason to doubt that the same effect could and does occur in the intrauterine patient, the fetus.
In Neurology of the Newborn, Dr. Volpe estimates that 12% to 23% of cerebral palsy is related to intrapartum asphyxia. Others give higher estimates. One study of 40 infants with documented seizures of various etiologies found that asphyxia was the most common cause of acute encephalopathy. Another authority on the subject has concluded that intrapartum asphyxia is a “major cause of acute mortality and chronic neurological disability in survivors.” He also noted that distinguishing infants suffering from intrapartum asphyxia from those with congenital diseases is relatively easy. The consequence of such morbidity is not insignificant; as stated by Dr. Volpe:
In view of the relatively high prevalence of cerebral palsy in most countries, generally 2 to 3 cases per 1,000 children born, even a relatively small percentage of cases caused by intrapartum events translates into a very large absolute number.
An interesting finding from one pertinent study was that infants born at night were more than twice as likely to die from asphyxia than those born during the day. The authors attributed that finding to “tiredness and inexperience of the night time staff, or a delay in appropriate treatment.” That same study found evidence from “confidential inquiries” into neonatal encephalopathy and deaths of term infants, that there had been a high proportion of “less than optimum care” during labor.
Relevant Cases
In the recent and important case of Tavares v. New York City Health and Hospitals Corporation, the defense sought a pretrial exclusion of the plaintiff’s experts’ opinions, characterizing them as medically unsound. Specifically, the defendants alleged that the plaintiff’s experts’ failure to adhere to the 4 “essential criteria” of Technical Bulletin 163 demonstrated a lack of general acceptance of such opinions. The Court made a detailed review of the pertinent medical literature, including the history behind Technical Bulletin 163 and NEACP, denied the defendants’ motion, and concluded:
...the theories advanced...that a rigid criteria of three or four factors must be present to find that cerebral palsy was caused by asphyxia or by a hypoxic event, are not generally accepted by the medical community as necessary to a diagnosis of neurological defect. Rather, plaintiffs have demonstrated that many authorities have indicated that the Apgar score and pH level are poor indicators of neurological defects and that not all infants born suffering from cerebral palsy have multiorgan involvement.
Further, the literature cited also demonstrates that Bulletin 163, the BMJ Template, and Chapter 8 have been criticized for lack of reliability. Based upon this analysis, it is determined that defendant has failed to establish that the theory relied upon by plaintiffs’ expert is novel and not generally accepted in the medical community, as is required by the Frye standard if the testimony is to be precluded....
Another important case on this issue is 1st Of America Bank v. USA. In a bench trial, the judge faced a similar challenge to the one presented to the court in Tavares, supra. The opinion testimony of several defense witnesses regarding causation had changed because of self-described “evolution” of their thinking. These defense experts initially attributed the minor plaintiff’s neurologic injuries to severe perinatal asphyxia; however, by the time of trial they had concluded that the cause of neurologic injury was unknown, but could not have been caused by perinatal asphyxia. That change in opinion was largely based upon the witnesses’ reading of the literature published by Karin Nelson, M.D. and Bulletin 163. The court found the reasoning behind the “evolution” of opinion suspect, as well as the underlying research which allegedly prompted the change in testimony, and ruled:
The Court finds these criteria of questionable value in litigation. If a court held a plaintiff to these criteria before finding causation as a result of perinatal asphyxia, plaintiff would be required to do more than demonstrate causation by a preponderance of the evidence. Plaintiff’s proof would have to be essentially conclusive.
Regarding the admissibility of questionable medical literature, generally, the case of O’Brien v. Angley , is instructive. The defense offered in evidence a portion of an editorial from the Journal of American Medical Association (JAMA). The trial court permitted its introduction as an exception to the hearsay rule pursuant to Rule 803 (18). The Ohio Supreme Court reversed holding that the editorial was primarily an expression of opinion on a controversial subject and was not a legitimate “learned treatise.” The Court held that where an:
author publishes an article with a view toward litigation, or where he possesses a personal interest in a litigable matter, a probability of bias exists which undermines the logic supporting the admission of this material in evidence as an exception to the rule against hearsay.
Conclusion
An objective review of the medical literature on the causes of cerebral palsy demonstrates that ACOG’s “essential criteria” are unreliable and not generally accepted in the medical community. Counsel should be alert to the need to challenge efforts to portray such literature as setting the standard for causation in birth injury cerebral palsy cases.
Reis Law, PLLC
66 Hanover St. Suite 203
Manchester, NH 03101
Ph: 603-792-0800