PATHOPHYSIOLOGYTwo divergent pathophysiological mechanisms forUCP have been described in the literature (29,30).Clark posited that normal fetal–placental circulationprotects the cord from prolapse by maintaining stiff-ness through turgor pressure. However, after repeatedor prolonged cord compression, the cord becomes limpand can more easily prolapse. More recently, Mc-Daniels et al (30) argued that acidemia is the causeand not the effect of cord prolapse. In their study,segments of umbilical cord from freshly deliveredplacentas were washed and then perfused with solu-tions of varying pH. Umbilical artery acidemia wasshown to increase the turgor of the umbilical cord. Incontrast to Clark (29), who argued that a stiff cordis less likely to prolapse, McDaniel posited that theincreased rigidity leads to decreased buoyancy andpredisposes the cord to prolapse