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)

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