In contrast, several investigators were not supportive of amnioinfusion for meconium staining. For example, Usta and associates (1995) reported that amnioinfusion was not feasible in half of women with moderate or thick meconium who were randomized to this treatment. These investigators were unable to demonstrate improved neonatal outcomes with this treatment. Spong and coworkers (1994) also concluded that although prophylactic amnioinfusion did dilute meconium, it did not improve perinatal outcome. Last, Fraser and colleagues (2005) randomized amnioinfusion in 1998 women with thick meconium-stained amnionic fluid in labor and found no beneits. Hofmeyr and associates (2014) reported mixed results from their review. Because of these indings, the American College of Obstetricians and Gynecologists (2016) does not recommend amnioinfusion to dilute meconium-stained amnionic fluid.
Studies that have attempted to correlate fetal heart rate patterns with brain injury primarily have examined infants identiied in medicolegal actions. Phelan and Ahn (1994) reported that among 48 fetuses later found to be neurologically impaired, a persistent nonreactive fetal heart rate tracing was already present at the time of admission in 70 percent. They concluded that fetal neurological injury occurred predominately before arrival to the hospital. When they looked retrospectively at heart rate patterns in 209 brain-injured newborns, they concluded that there was not a single unique pattern associated with fetal neurological injury (Ahn, 1996). Graham and associates (2006) reviewed the world literature published between 1966 and 2006 on the efect of fetal heart rate monitoring to prevent perinatal brain injury and found no beneit.
Fetal heart rate patterns necessary for perinatal brain damage have been studied in experimental animals. .1yers (1972) described the efects of complete and partial asphyxia in rhesus monkeys. Complete asphyxia was produced by total occlusion of umbilical blood low that led to prolonged deceleration (Fig. 24-26). Fetal arterial pH did not drop to 7.0 until approximately 8 minutes after complete cessation of oxygenation and umbilical low. At least 10 minutes of such prolonged deceleration was required before there was evidence of brain damage in surviving fetuses.
Myers (1972) also produced partial asphyxia in rhesus monkeys by impeding maternal aortic blood flow. This resulted in ...A �EEI0). /0 5 1005 10 Asphyxia (min) 0.
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FIGURE 24-26 Prolonged deceleration in a rhesus monkey shown with blood pressure and biochemical changes during total occlusion of umbilical cord blood flow. (Data from Myers, 1972.) analgesia was used in 55 percent. The length of the second stage, even in those lasting up to 6 hours or more, was not related to neonatal outcome. These results were attributed to careful use of electronic monitoring and scalp pH measurements. These investigators concluded that there is no compelling reason to intervene with a possibly diicult forceps or vacuum extraction because a certain number of hours have elapsed. They observed, however, that after 3 hours in the second stage, delivery by cesarean or other operative method increased progressively. By 5 hours, the prospects for spontaneous delivery in the subse quent hour were only 10 to 15 percent.
Newer guidelines have been promoted by the Consensus Com mittee (2016) for second-stage labor. These recommend allowing a nullipara to push for at least 3 hours and a multipara to push for at least 2 hours before second-stage labor arrest is diagnosed.
One caveat is that maternal and fetal status should be reassuring.