Birth Injuries

Evaluation of a " Birth Injury " Case, Part II (Continued)

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.

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