By Russell Gregory
Birth-trauma cases typically involve claims of brain injury. The injuries are often quite severe and, correspondingly, the stakes are high. Accordingly, these cases are vigorously prosecuted and defended.
In such cases, a great deal of time is spent analyzing medical literature regarding causation of perinatal, or birth-related, brain injury. Countless volumes have been written on the subject in various fields of medicine, such as perinatology, neonatology and pediatric neurology.
However, a document published in 1992 by the American College of Obstetricians and Gynecologists (ACOG) has gained particular notoriety in the birth-injury litigation community. This document — Technical Bulletin No. 163, Fetal and Neonatal Neurologic Injury — has become the pillar of causation defense in birth-trauma litigation.
Basically, TB 163 asserts that brain injury cannot be attributed to birth-related events unless four elements are present in the immediate newborn period:
- profound umbilical artery metabolic or mixed acidemia (pH less than 7.00);
- persistence of an Apgar score of 0-3 for longer than five minutes;
- neonatal neurologic sequela, e.g., seizures, coma, hypotonia; and
- multi-organ system dysfunction, e.g., cardiovascular, gastrointestinal, hematologic, pulmonary, or renal.
For ease of reference hereinafter, the four items listed above will be referred to as low pH, low Apgars, seizures, and multiorgan dysfunction, respectively.
Regarding attributing brain injury to perinatal events, the Technical Bulletin states that "all of the following criteria [listed above] must be present before a plausible link can be made." (See, Technical Bulletin, p. 2.) In cases where all four criteria are not met, the defense asserts TB 163's mandatory language as definitive that the claimed brain injury could not have resulted from birth. This assertion is sometimes made via motion for summary disposition under the Davis-Frye doctrine, requiring that causation expert testimony be supported by "recognized scientific knowledge." (For a discussion of this doctrine and its application, with relevant case citations, see Anton v. State Farm, 238 Mich. App. 673, 607; N.W.2d 123 (1999).) 
Much has been written vehemently questioning both the scientific support for and the motive behind promulgating TB 163. (See, Goodlin, R.C., M.D., "Do Concepts of Causes of Prevention of Cerebral Palsy Require Revision?" Am. J. Of Obstet. and Gynecol., Vol. 172, No. 6, June 1995; Tilson, J.L., J.D., "Exposing Manufactured Scientific Literature," MTLA Quarterly, Summer 1994, pps. 12-16; Morgan M.D., J.D., "Obstetrical Medical Malpractice"; Bartemus, J., J.D., ACOG 163 "Fetal and Neonatal Neurological Injury: Fact or Myth?" (outline of perinatal conference presentation).)
Certainly, it is interesting that an obstetrical body (ACOG) purportedly laid to rest in three pages what other specialities focused principally upon causation have been unable to clearly delineate in decades of modern scientific research and debate. Nonetheless, it is not the focus of this writing whether TB 163 was properly substantiated or motivated. This exposé addresses only whether there is literature support for the proposition that perinatal brain injury can occur without some or all of the purported sine qua non factors listed above. If so, this suffices to meet the "recognized scientific knowledge" test of admissibility. (See, Anton, supra.)
This author has encountered the defense argument that, while a plaintiff may not have exhibited all of the four neonatal parameters, at least some combination of them is requisite to attributing the brain injury to the perinatal period. While seemingly reasonable, this line of thinking is fallacious.
Consider this: If "A" is not requisite and "B" is not requisite and "C" is not requisite and "D" is not requisite, how can any combination of these — or even any one of these — be requisite? Obviously, they cannot. Therefore, it is important to look at whether literature exists stating that one or more of the four parameters is not requisite.
As discussed below, literature in fact exists finding each of the four parameters to be non-requisite. Recognized scientific knowledge exists, as demonstrated in the literature, that perinatal hypoxic ischemic injury can occur in the absence of these factors.
Low PH
Absent adequate oxygenation, tissue cells utilize glucose as a metabolic substrate. Glucose metabolism produces lactic acid as a by-product. This acid, released into the blood stream, produces a drop in the pH (acidosis).
Whether and to what extent a measurable drop will occur depends upon how much lactic acid is produced and when, relative to the pH measurement, the production occurs (allowing time for the lactic acid to osmose from cells into the blood stream and circulate into the umbilical cord). These factors will be influenced by the timing and severity of the oxygen deprivation. Likewise, a given fetus' tolerance for oxygen deprivation will vary according to many factors, including gestational age, prior in utero stresses, infections, metabolic rates, heredity.
All of these factors are sliding scale parameters. It is not surprising, therefore, that "most neonates with hypoxic-ischemic encephalopathy are not acidotic at birth." (Emphasis added.) (Schifrin, B.S., M.D., "Antenatal Fetal Assessment: Overview and Implications for Neurologic Injury and Routine Testing," Clinical Obstetrics and Gynecology, Vol. 38, No. 1, pps. 132-41, 1995, J.B. Lippincott Co., citing Low, J.A., M.D., "The Role of Blood Gas and Acid-Base Assessment in the Diagnosis of Intrapartum Fetal Asphyxia," Am. J. Obstet. Gynecol., 1989, 159: 1235-40.)
Indeed, "normal umbilical cord acid-base and blood gas values may be obtained from a fetus that dies as long as ten minutes before birth." (Emphasis added.) (Nakamura, K.T., M.D., Smith, B.A., M.D., Erenberg, A, M.D., Robillard, J.E., M.D., "Changes in Arterial Blood Gases Following Cardiac Asystole During Fetal Life," Obstetrics and Gynecology, Vol. 70, No. 1, July 1987, p. 17.)
Thus, there is clearly recognized literature support for the proposition that low pH is not requisite.
Low Apgars
Newborn Apgar scores measure functions controlled by the brain stem such as tone, reflex irritability, respiratory effort, color and heart rate, rather than the higher lobes of the brain. Thus, it is well known that anencephalic babies — those born without higher lobes of the brain — can have good Apgar scores at birth.
Decreased fetal cerebral circulation which adequately perfuses the brain stem, but inadequately perfuses the distal-most portions of the cerebral arterial tree (the watershed), spares the brain stem, notwithstanding injury to the distal-most perfused brain centers. Thus, it is not surprising that "newborn infants with perinatal hypoxic injury to higher centers may retain brain stem function and have reasonable Apgar scores." (Schifrin, B.S., M.D. "The ABCs of Electronic Fetal Monitoring," Journal of Perinatology, Vol. XIV, No. 5, 1994, p. 397.) Moreover, "asphyxia can exist in an apparently vigorous baby." (Danforth's Obstetrics and Gynecology, 7th Ed., 1994, p. 124.)
Clearly, there is literature support that low Apgars are not requisite.
Seizures
Neonatal seizures due to hypoxia ischemia are most thought to be due to brain swelling. Volpe notes that, unlike the adult brain, the newborn brain appears to be increasedly resistant to brain swelling from hypoxic-ischemic insult. Thus, he states that "it is reasonable to ask whether brain swelling (and thus consequent seizure activity) with hypoxic-ischemic injury is a consistent feature in the human newborn with perinatal asphyxia." (Volpe, J.J., M.D., "Neurology of the Newborn," 3d Ed., 1995, p. 279.)
Notably, even where seizure activity does exist, it is often subtle and missed in newborns. G.M. Fenichel, M.D., in "Clinical Pediatric Neurology: A Signs and Symptoms Approach," (3d Ed., 1997, Chapter 1, p. 1) states that "seizures in newborns, especially those who are premature, are poorly organized and difficult to distinguish from normal activity."
Further, Creasy & Resnik, in "Maternal-Fetal Medicine: Principles and Practice," (3d Ed., 1994, p. 1166) states, "... the true incidence (of neonatal seizures) maybe obscured by the fact that in many infants, the manifestations are extremely subtle and may not be recognized."
Additionally, "…many electrographic seizures are not accompanied by clinically observable alterations in neonatal motor or behavioral function; this finding suggests that the total number of neonatal seizures may have been underestimated in the past" and "…the clinical manifestations of certain neonatal seizures are readily and frequently overlooked …." (Volpe, supra, pp. 178-79.)
Clearly, there is recognized scientific knowledge that documented seizures are not requisite. Moreover, note that TB 163 considers not only seizures a fulfillment of this category, but other indications of diminished neurological status as well, including mere hypotonia.
Multiorgan System Dysfunction
Multiorgan system dysfunction occurs when blood flow, as a brain-saving bodily response, is preferentially shunted to the brain, sparing the brain at the expense of less vital organs. At this point, it is quite clear and undisputed in the literature that acute (near the time of birth) significant diminished fetal cardiac output will injure the brain before the shunting mechanism and/or organ injury therefrom occurs.
In "Intrapartum Fetal Asphyxial Brain Injury With Absent Multiorgan System Dysfunction" (Phelan, J.P., M.D., Ahn, M.O., M.D., Ph. D., M.P.H., Korst, L, M.D., Martin, G.I., M.D., and Wang, Y., M.D., Ph. D. J. Of Maternal-Fetal Medicine, 7:19-22 (1988)), the authors assert that "[t]hese acute injuries, associated with a prolonged fetal heart rate deceleration, may be linked to severely decreased cardiac output and hypotension that caused vulnerable portions of the brain to be injured before other organs."
Furthermore, R. Vannucci, M.D., in "The Central Nervous System, Neonatal-Perinatal Medicine," (Fanaroff and Martin) at p. 887 said, "Occasionally, newborns who have suffered asphyxia severe enough to produce brain damage do not exhibit symptoms, signs or laboratory evidence of multi-focal organ injury. Typically, such infants are those who have sustained a short-lived (minutes) but near total asphyxia secondary to acute abruption of the placenta, umbilical cord prolapse, or other disturbance. Severe cardiovascular depression with systemic hypotension (shock) and total body ischemia, including brain ischemia, rapidly ensues. Because the systemic hypotension is immediate and profound, a redistribution of blood flow from non-vital (heart, brain) organs does not occur. Accordingly, the brain bears the brunt of the injury, even in the absence of ischemic changes in other organs."
Meanwhile, "The Syndrome of Acute Near-Total Intrauterine Asphyxia in the Term Infant," authors J.F. Pasternak, M.D., and M.T. Gorey, M.D., (Pediatric Neurology, May 1988, 18 (5): 391-98) state that the higher metabolic rate of the brain compared with other organs explains the injury to the brain while the other organs are spared. Thus, there is recognized scientific literature stating that multiorgan dysfunction is not requisite.
Perinatal Hypoxic-Ischemic Brain Injury
It should be noted that perinatal hypoxic-ischemic brain injury can occur in the absence of any, or any combination of, the four alleged requisite factors. Findings such as those indicated above, rendering the alleged requisite factors non-requisite, have caused pre-eminent publishing physicians to conclude that these four factors are simply not appropriate measuring sticks to determine whether perinatal hypoxic-ischemic brain injury has occurred.
Korst, et al., notes as follows: "[d]espite their valiant efforts, we were unable to show a plausible link between these criteria and intrapartum fetal CNS (central nervous system) injury." (Emphasis added.) (Korst, L.M., M.D., et al., "Can Persistent Brain Injury Resulting From Intrapartum Asphyxia Be Predicted by Current Criteria?" Perinatal-Neonatal Medicine, Vol. 2, 1997. pps. 286-93.)
Not even a plausible link! Not surprisingly, it has been determined that "currently used indicators to define permanent fetal brain injury [the four TB 163 parameters] are not valid." (Korst, L.M., M.D., Phelan, J.P., M.D., Wang, Y, M.D., Martin, G.I., M.D., Ahn, M.O., M.D., "Acute Fetal Asphyxia and Permanent Brain Injury: A Retrospective Analysis of Current Indicators," Journal of Maternal-Fetal Medicine, May-June, 1999, 8 (3): 101-06.)
The same article states, at pps. 104-05, that "[s]everely neurologically impaired neonates with evidence of intrapartum asphyxia failed to consistently satisfy the four criteria for attributing their brain injury to the intrapartum period (citation). Individually, each of these criteria has been criticized (citation), yet the authors of the intrapartum asphyxia criteria emphasize that these criteria taken together should more accurately identify those neonates injured during the birth process (citation). As before in a heterogeneous population (citation), ACOG Technical Bulletin No. 163 (citation) was not found to be valid in an acute intrapartum asphyxial model."
Most importantly to the evidentiary issue, it has been concluded unequivocally that acute fetal hypoxic-ischemic injury occurs absent any of the four alleged requisite factors. (Id. at 104, Fig. 1.)
Note that the majority of the references cited herein are to leading authors and publications in their respective fields.
Of course, it makes intuitive sense that focal and multi-focal brain injuries (e.g., watershed injuries) will not produce global neonatal dysfunction. As Schifrin points out, "Because ischemia to the brain and other organs (that is, localized asphyxia), not systemic global asphyxia, appears to be the major precursor of human fetal injury, it seems unreasonable to insist upon systemic fetal asphyxia at any time to validate the timing or mechanism of fetal injury." (Schifrin, supra, (ABCs), p. 401.)
Thus, Schifrin concludes, "[n]or can we use the absence of one or more of these signs to exclude perinatal asphyxia as the cause of injury." (Id.)
Conclusion
It should be noted that the author has been on both sides of the fence, defending and prosecuting birth-trauma cases.
But whatever one's orientation or personal opinion, it is undeniable that there is "recognized scientific knowledge" that diminished fetal brain perfusion during labor and delivery may result in permanent, severe neurologic injury absent all, or even any one, of the four TB 163 parameters. This is sufficient to render expert causation testimony in this regard admissible.
Russell Gregory is a principal of Gregory & Reiter, P.C., also known as American Baby & Child (ABC) Law Centers in Farmington Hills, which deals exclusively with birth-trauma cases. The author would like to thank to his partner, Jesse Reiter, and associate, Scott Weidenfeller, for their contributions to this article. Gregory can be reached at (248) 473-8800.
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September 18, 2000
