Induction of labor and intrapartum fetal distress

Many cases also arose in the context of induction of labor for pre-eclampsia with the subsequent development of intrapartum ''fetal distress.'' The alleged ''fetal distress'' resulted in a brain-damaged infant or an intrapartum fetal death. When a decision is made to intervene by induction of labor for pre-eclampsia, each pregnancy should be assessed for the prospects of safe vaginal birth. If, for example, there is clinical evidence of intrauterine growth impairment and/or oligohydramnios, Cesarean may be the preferred route of delivery to avoid the downstream consequences of abruption and/or intrapartum fetal distress.

If induction of labor for pre-eclampsia is, nevertheless, undertaken, the fetus should be monitored during labor. As noted in these case summaries, 4 (17%) cases appeared to have preadmission fetal brain injury, 1 (4%) case described a FHR pattern consistent with the Hon pattern of intrapartum asphyxia, and several cases had a sudden, rapid and sustained deterioration of the fetal heart rate due to abruption or recurrent maternal seizures (Greenberg etal, 2001; Phelan and Ahn, 1994, 1998; Phelan and Kim, 2000; Phelan et al., 2001; Schifrin etal., 1994).

In Dans v. Rappaport (2000), for example, the gravida was being followed prenatally for suspected pregnancy-induced hypertension and possible pre-eclampsia. On the morning of delivery, she was 35 weeks gestation and she noted that her fetus did not move. That day, she was evaluated by her obstetrician. A nonstress test (NST) done during that visit was considered nonreactive. Later the same day, she was admitted to the hospital. At the hospital, the FHR pattern continued to be nonreactive. Approximately 6h after the NST in the obstetrician's office the infant was delivered by Cesarean section. During this

6-hour period, the FHR, according to the facts, remained nonreactive with an absence of FHR accelerations, and a normal baseline rate of 120-130 bpm.

At birth, the infant had Apgars of 0 and 1 at one and five minutes, respectively, with an umbilical artery pH of 6.8. Additionally, an extremely elevated nucleated red blood cell count was noted in the neonate. An MRI taken at 7 years of age demonstrated white matter injury in the periven-tricular region. As of the time of the verdict, the child was permanently neurologically impaired.

This case manifests many of the findings in fetuses with a preadmission CNS insult. For example, the fetus did not move or had stopped moving prior to the maternal visit to the obstetrician's office. In the usual circumstance, the fetus that does not move is presumed to be dead. In this case, the fetus by virtue of a nonreactive FHR pattern was alive. The finding of decreased or absent fetal movement is in keeping with the observations of Schifrin et al. (1994) and Phelan and Kim (2000). These investigators found a significant increase in reduced or absent fetal activity among pregnancies complicated by a preadmission fetal brain injury.

Additionally, this fetus had a persistent nonreac-tive FHR pattern over a 6-hour period. This finding is also in keeping with the literature (Greenberg et al., 2001; Phelan, 1998; Phelan and Ahn, 1994; Phelan and Kim, 2000; Phelan et al., 2001). In the absence of a rising baseline FHR in association with repetitive FHR decelerations or a sudden, rapid and sustained deterioration in the FHR unresponsive to remedial measures that lasts until delivery, the fetal brain injury is probably consistent with a static encephalopathy (Greenberg etal., 2001; Phelan andAhn, 1994,1998; Phelan and Kim, 2000; Phelan et al., 2001).

While the case discussion provides solely that the NRBC values were ''extremely elevated,'' fetuses with preadmission brain injury have been linked to elevated NRBC (Korst et al., 1996; Phelan et al., 1995, 2003). An association has been shown between elevated NRBC and persistent nonreactive FHR patterns intrapartum and with indirectly reduced or absent fetal movement. (Ghosh et al., 2003; Korst et al., 1996; Phelan et al., 1995, 2003.)

Thus, the Dans matter, though decided in favor of the plaintiff, was consistent with a preadmission neurologic insult and inconsistent with an acute intrapartum insult because of the persistent nonreactive FHR pattern, the elevated NRBC, the neuroimaging showing white matter injury, and the absence of fetal movement (Phelan and Kim, 2000).

In the Novell case (Novell v. Community Hospital of Central California, 1999) of fetal brain damage due to an apparent Hon pattern of intrapartum asphyxia (Phelan and Kim, 2000; Phelan and Ahn, 1994, 1998), a 22-year-old gravida was admitted at 37 weeks gestation for induction of labor due to pre-eclampsia. After 22 h of oxytocin-induced labor, the certified nurse midwife consulted with the obstetrician about performing a Cesarean section. The OB decided to increase the oxytocin. By 7:00 A.M., the FHR had gradually increased to 180 bpm in association with a maternal fever. As a result of the fever, the mother was treated with antibiotics. At 7:50 A.M., the FHR fell to 60 bpm for longer than 6 min. The patient was scheduled for a Cesarean delivery. In the meantime, the patient was given terbutaline for intrauterine fetal resuscitation. The fetus recovered to a rate of 180 bpm. By 8:20 A.M., the FHR was now over 200 bpm; and, the fetal head was at a +2 station. The OB decided to have the mother push in an effort to deliver the fetus vaginally. At 9:30 A.M., the OB decided to do a vacuum delivery. At 9:45 A.M., the vacuum was applied. The fetal head delivered at 10:02A.M. and the body followed at 10:05A.M. During the vacuum delivery, variable decelerations were observed; and, these decelerations culminated in a terminal bradycardia. At birth, the infant had Apgars of 0, 0, and 0 at 1, 5, and 10 min, respectively; and, an umbilical arterial pH of 7.02. The long-term followup of the infant demonstrated profound brain damage with a feeding gastrostomy and a tracheostomy.

This case illustrates a probable Hon pattern of intrapartum asphyxia (Phelan and Ahn, 1994, 1998; Phelan and Kim, 2000). The characteristics of this pattern are illustrated in Figure 34.2. As noted in the Novell case (Novell v. Community Hospital of Central California, 1999), the maximum FHR was 200 bpm from a previously normal tracing. In a situation such as this, the obstetrician and nurse should be asking themselves why the fetal heart rate or fetal cardiac output has risen to such a level during labor. Could the entire change in FHR be attributed to the maternal fever or is the fetus becoming asphyxiated? In the end, the fetus appeared to be unable to maintain its cardiac output, resulting in a terminal bradycardia.

In the setting of a Hon pattern of intrapartum asphyxia and maternal pyrexia, antibiotics and antipyretics should be administered. If the fetus does not revert to a normal tracing, similar to the one seen on admission, within a reasonable period of time, delivery should be accomplished in the most expeditious manner.

Sentinel hypoxic events in some, but not all, of these pre-eclampsia cases arose in the context of a maternal arrest or an abruption (MacLennan, 1999). Intrapartum, these sentinel events appeared to produce a sudden, rapid, and sustained deterioration of the fetal heart rate lasting until delivery after an apparently normal initial tracing.

The key distinction among ''acute fetal distress'' cases relates to whether the condition singularly affects the fetus, such as an abruption, or is the ''fetal distress'' due to a maternal arrest. Under the circumstances of a maternal arrest, maternal health overrides fetal health. Thus, if a pregnant pre-eclamptic patient sustains a cardiopulmonary arrest, cardiopulmonary resuscitation (CPR) should be initiated immediately. For efficient CPR, the patient should be supine and the uterus displaced laterally to optimize maternal cardiac output. Once CPR is initiated, the timing of the Cesarean is critical to enhance maternal and fetal outcome. According to Katz and associates (1986), ''Cesarean

180 FHR

Fetal Ischemia

180 FHR

-Nonreactivity ^v. -Increasing baseline rate A -Repetitive decels \ -Loss of variability >v



-Decreasing baseline rate -Stair-steps to death -Fetal death


Figure 34.2 The characteristics of the Hon pattern of intrapartum asphyxia are represented. The pattern begins with a reactive admission fetal heart rate followed by nonreactivity, a progressive and substantial rise in the baseline rate to a level of tachycardia in association with repetitive decelerations and usually diminished variability.

delivery should be begun within 4 minutes, and the baby delivered within 5 minutes of maternal cardiac arrest.'' CPR should be continued throughout and after the delivery.

The fourth context in which fetal brain injury or death arose was in the eclamptic patient. As noted in the Gold matter (Gold v. United Health Services Hospital, 1998), the patient developed multiple seizures in association with FHR decelerations. Subsequently, the infant was delivered and later noted to be permanently neurologically impaired with spastic quadriplegia.

Maternal seizures are a well-known but infrequent sequel of pre-eclampsia. Maternal convulsions require prompt attention to prevent harm to both mother and fetus (Naidu et al., 1996; Paul et al., 1978; Pritchard et al., 1984). During a seizure, the fetal response is usually manifested as an abrupt, prolonged FHR deceleration (Paul et al., 1978). During the seizure, which generally lasts less than 1—2min (Paul et al., 1978), transient maternal hypoxia and uterine artery vasospasm occur and combine to produce a decline in uterine blood flow. In addition, uterine activity increases secondary to the release of norepinephrine, resulting in an additional reduction in uteroplacental perfusion. Ultimately, the reduction of uteroplacental perfusion causes the FHR deceleration. Such a deceleration may last up to 9 min (Paul et al., 1978). Following the seizure and recovery from the FHR deceleration, a loss of variability and a compensatory rise in baseline FHR are characteristically seen. Transient late decelerations are not uncommon but resolve once maternal metabolic recovery is complete.

The cornerstone of patient management during an eclamptic seizure is to maintain adequate maternal oxygenation and to administer appropriate anticonvulsants. After a convulsion occurs, an adequate airway should be maintained and oxygen administered. To optimize uteroplacental perfusion, the mother should be repositioned onto her side. Anticonvulsant therapy with intravenous magnesium sulfate (Naidu et al., 1996; Pritchard et al., 1984) to prevent seizure recurrence is recommended. In spite of adequate magnesium sulfate therapy, adjunctive anticonvulsant therapy occasionally may be necessary (Pritchard et al., 1984). In the event of persistent FHR decelerations, intrauterine resuscitation with a betamimimetic (Arias, 1978) or magnesium sulfate may be helpful in relieving eclampsia-induced uterine hypertonus. Continuous electronic fetal monitoring should be used to follow the fetal condition. It is also axiomatic in this circumstance of conflicting maternal and fetal interests that maternal interests take precedence over those of the fetus (Phelan, 1991). This means the first step is to stabilize the seizing pregnant woman. After the mother has been stabilized, and if the fetus continues to show signs of distress after a reasonable period of recovery, delivery in the most expeditious manner should be considered.

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