Any attorney contemplating a birth-injury case must anticipate the defenses, both legitimate and illegitimate, that can be raised in such claims. Indeed, an intelligent decision to undertake a birth-injury claim cannot be made without an examination of all the various factors that make it more or less likely that the claim will succeed. These factors can be clinical, scientific and theatrical. In this issue I will speak only to the clinical and scientific factors that play an important role in the prosecution and defense of birth-injury claims.
The clinical management of a pregnancy or delivery is not unlike the clinical management of other conditions in disease and in health. While almost invariably, an anticipated or expected course exists, there are also anticipated or expected variations from the usual course. There are melodies and there are variations. A skilled and careful listener should readily recognize the harsh note or a change in key or rhythm.
Similarly, a pregnancy has a usual course. Gestation is generally 40 weeks and the course of gestation is considered normal unless the period of gestation is significantly shorter or longer. However, even if the period of gestation is either significantly shorter or significantly longer, a healthy, normal baby usually is born. A post-dates (prolonged) gestation at 42 weeks, plus, is a pregnancy at greater risk than a pregnancy at 40 weeks gestation but it is, nevertheless, the case that the overwhelming majority of post-dates children at 42, 43 and even at 44 weeks gestation are born without permanent adverse consequences. The same can be said of children who are born prematurely. The advances in neonatal medicine now make it possible to predict that the majority of children born at 26 weeks gestation will survive without permanent harm.
The different approaches in managing pregnancy, labor and delivery that are undertaken for prematurity, post-dates, or other disorders, are crafted in recognition of the specific risks for each individual situation with a view toward reducing or eliminating those risks. Nevertheless, defense experts in birth-injury cases will commonly condemn or trivialize those measures universally employed to reduce the risk of injury to mother and child. For example, electronic fetal monitoring is the standard of practice in the United States. It is the gold standard by which any other form of monitoring must be measured. Nevertheless, defense experts will routinely deride the significance of ominous fetal heart tracings unless an “ominous” meaning is consistent with the defense of a particular health care provider.
Electronic fetal monitoring is a very sensitive indicator of fetal well being. It is however a better indicator of distress than it is of fetal injury. It’s value as a monitoring device is based on its great sensitivity. Health care providers who ignore the warning provided by traditional ominous fetal heart monitoring patterns do so at the peril of their patients (and at their own peril in court).
The causation defense of birth injury cases has evolved over the years and is, in fact, constantly changing. Whereas, once the causation defense was restricted primarily to the type of the injury produced and the condition of the baby at the time of birth, today the defense touts a variety of theories that purportedly enables their experts to not only accurately predict the time when a birth injury occurred, but to always find that time for preventing injury by medical intervention is essentially non-existent. The window of time during which intervention might help is always before or after any defendant had any possible opportunity to act.
The “narrow window” defense has many disguises. These disguises are based on defense experts’ claims as to either the mechanism of injury or the timing of injury.
Legitimate defenses exist within the mechanism of injury defense. For example, a completedembolic stroke occurring in utero is a rare but unheralded event and the injuries caused by it are not preventable. True congenital brain disorders such as trisomy 21 are sometimes preventable by prenatal and/or genetic counseling and testing but are not a result of the labor process. However, it is popular today for a defense expert to claim that intrauterine infection “chorioamnionitis” causes injuries in utero by a mechanism that cannot be identified by health care providers prior to injury occurring and that such injuries cannot be prevented. This, in my view, is an illegitimate claim.
The scientific evidence for brain injuries resulting from an infection in the amnion is limited. [Neurologic sequelae of streptococcal infection are beyond the scope of this paper.] It is important to be aware, however, that authors such as Grether and Nelson, have claimed in the literature that chorioamnionitis is a risk factor for neonatal outcomes commonly attributed to birth asphyxia.(1)
Fortunately, in August of 1999, a massive retrospective cohort study published out of the University of Texas, Southwestern Medical Center, Dallas, Texas, provides strong evidence to the contrary. A total of 101,170 term infants were analyzed. Fully 5% of the infants were born to women with chorioamnionitis (5,144). After adjustment for confounding factors, it was clear that neurologic morbidity was not related to maternal infection during labor but rather was significantly related to other labor complications.(2)
Defense experts hypothesize a variety of esoteric mechanisms to support their claim chorioamnionitis produces irreversible untreatable injuries in utero. Adverse consequences result, they claim, from cytokines, a chemical attractant elaborated by inflammatory cells to recruit other inflammatory cells to the site of infection. The proponents of the brain injuring effects of cytokinesia claim that the cytokines produce brain injury by direct effect on brain tissue and/or by vasoconstriction of blood vessels.
This theory that cytokinesia causes brain damage remains unproven, but most enlightened proponents or advocates of this theory concede that the hostile environment created in utero by cytokinesia resulting from chorioamnionitis is an environment having progressive consequences. To the extent that cytokinesia may over time have neurologic consequences simply places it in the category of the other presently known mechanisms accounting for how infants are injured by delays in the recognition of distress and delays in the delivery of infants from hostile environments.
A more dangerous, and in my view, illegitimate use of the cytokinesia theory is to claim as some few defense witnesses do, that cytokinesia causes a brief interval of vasoconstriction sufficient to cause permanent and enduring neurologic sequelae and, thereafter, has no further effect. There is no literature supporting this hypothesis.
Another mechanism for brain injury that has been used as a part of the “narrow window” defense is meconium induced umbilical cord vasoconstriction. Some proponents of this theory in the medical literature have avidly argued that some benign event might cause a baby to pass meconium and that, in some babies, the passage of meconium would result in umbilical cord vasoconstriction which, after a brief interval of 12 to 16 hours, would dissipate. The persistence of meconium would thereafter cause no adverse consequence and a practitioner would have no opportunity to prevent the injury done by the meconium by earlier delivery. Not surprisingly, these defense witnesses always seem to have some way of proving that the meconium must have been passed prior to any opportunity for earlier delivery and treatment.
Altschuler and others, attempting to prove this hypothesis through in vitro experimentation, subjected umbilical cords to increasing concentrations of meconium.(3)
Much to their surprise, they discovered that umbilical vasoconstriction did not occur at any concentration of meconium unless the meconium was introduced directly into an umbilical artery. On the other hand, it is generally known that sterile water introduced into an umbilical artery will also cause vasospasm.
Various components are present in the blood of newborns. In the medical literature, numerous authors attempt to answer the question of whether the examination of the quantity of a particular blood element or the timing at which a certain quantity of that blood element is present or the process by which the blood element increases or dissipates in its concentration, reveals the time when a brain injury has occurred. Such efforts have been made with reference to platelets, NRBC’s and lymphocytes. Certain defense experts, claim that an infant having a platelet count of 185,000 when born has, by reason of this platelet count, been injured prior to the mother’s labor admission. There is no scientific evidence in the medical literature ascribing such a significance to platelets. In fact, the general pediatric literature makes clear that such levels of platelets are normal.
Other defense experts rest their timing defenses on the appearance of nucleated red blood cells. Legitimate medical evidence supports the proposition that nucleated red blood cells can be found in increased numbers at some point following a hypoxic stimulus. Any defense expert who claims that he or she can predict the timing of a hypoxic stimulus based on the level of nucleated red blood cells present at some point in time, is basing the conclusion upon fantasy. Benirschke, in his text Pathology of the Human Placenta, Third Edition, analyzes the folly of such positions. Benirschke points to his own experience that has shown a significant elevation in nucleated red blood cells occurring shortly after hypoxic insult. The literature contains examples of cases where a longer interval between hypoxic insult and elevation was observed.
The leading advocate of basing the timing of hypoxic insult on the appearance and level oflymphocytes and the timing of their decline has conceded in sworn testimony in various cases to irregularities in his data. Because of these admitted irregularities, a Pennsylvania court, on a Frye motion has excluded the conclusions of the defense expert.(4)
There are no other studies on the subject at this time.
One must take nothing for granted. The standards of practice upon which a liability case is based are derived from a current informed understanding of the underlying pathophysiologic mechanisms by which particular injuries occur. As usual, a false premise lacking a principled and honest foundation, is easily revealed. It is our job to show this emperor has no clothes.
1 Grether, J.K., Nelson, K.B., “Maternal Infection in Cerebral Palsy in Infants of Normal Birth Weight,” JAMA 1997; 278: pp. 207-11.
2 Alexander, J.M., McIntire, D.M., and Leveno, K.J., “Chorioamnionitis in the Prognosis for Term Infants,” Obstetrics and Gynecology, Vol. 94, No. 2., August 1999, pp. 274-278.
3 Pickens, J.; Toubas, P.; Hyde, S.; Altshuler, G.; “In vitro Model of Human Umbilical Venous Perfusion to Study the Effects of Meconium Staining of the Umbilical Cord,” Biol. Neonate 1995; 67(2): pp. 100-108.
4 Linda Clemens and Michael Clemens, parents and natural guardians of Rayel Clemens, a minor, vs. David Gillum, M.D., James L. Wilson, M.D. and Soldiers and Sailors Memorial Hospital. In the Court of Common Pleas of Tioga County, Pennsylvania, No. 508 of 1994.