Intrapartum Fetal Assessment and Therapy

Abstract

Accurate fetal assessment in labor remains challenging despite the application of new technologies. An elevated cesarean delivery rate and persistent cases of fetal/neonatal neurologic injury indicate the need to further optimize fetal/neonatal outcomes while minimizing unnecessary maternal interventions.

Keywords

Electronic fetal heart rate monitoring, Intrapartum stillbirth, Intrapartum fetal assessment, In utero resuscitation, Fetal acidemia

Chapter Outline
Fetal Risk during Labor, 155
Intrapartum Fetal Assessment, 156
- Electronic Fetal Heart Rate Monitoring, 156
- Limitations of Electronic Fetal Heart Rate Monitoring, 160
- Methods for Improving the Efficacy of Electronic Fetal Heart Rate Monitoring, 162
- Supplemental Methods of Fetal Assessment, 162
- Additional Technologies for Fetal Assessment, 163
- Research Technologies for Fetal Assessment, 164
Intrapartum Fetal Therapy, 164

Accurate fetal assessment in labor remains challenging despite the application of new technologies. An elevated cesarean delivery rate and persistent cases of fetal/neonatal neurologic injury indicate the need to further optimize fetal/neonatal outcomes while minimizing unnecessary maternal interventions.

Fetal Risk during Labor

The fetus is at risk during labor and delivery. Worldwide, intrapartum stillbirths account for almost 1.3 million perinatal deaths per year, with a range of 10% to 50% of all stillbirths in developed and developing countries, respectively. Obstetric care can influence the intrapartum stillbirth rate. With each percentage increase in cesarean delivery rate up to 15%, intrapartum stillbirth rates decrease by 1.61/1000.

Experimental models support the hypothesis that intrapartum events can have long-term neurologic sequelae for the offspring. Fetal monkeys subjected to hypoxia in utero suffer neurologic injuries similar to those seen in children who presumably suffered asphyxia in utero . Work with rodent, rabbit, piglet, and sheep models have shown similar patterns of damage.

Some fetuses appear to be at greater risk for adverse intrapartum events than others. Older studies report that high-risk mothers constitute 20% of the pregnant population, but their offspring represent 50% of the cases of perinatal morbidity and mortality. Various methods for identification of high-risk pregnancies have been published. High-risk pregnancies include, but are not limited to, women with (1) medical complications (e.g., hypertension, preeclampsia, diabetes, autoimmune disease, hemoglobinopathy); (2) fetal complications (e.g., fetal growth restriction, nonlethal anomalies, preterm delivery, multiple gestation, post-datism, hydrops); and (3) intrapartum complications (e.g., abnormal vaginal bleeding, maternal fever, meconium-stained amniotic fluid, oxytocin augmentation of labor). Owing to inadequate sensitivity, poor positive predictive values, and the inability to modify risk factor–related outcomes, high-risk scoring systems have not been proven to improve pregnancy outcomes. In one study, more than half of infants with asphyxia had no clinical risk factors. However, scoring systems may be useful in the management of low-risk parturients who do not warrant continuous monitoring during labor. One European strategy for identifying high-risk parturients integrates the analysis of the fetal heart rate (FHR) tracing at the time of admission; if the FHR tracing is abnormal, patients receive intensive monitoring. A meta-analysis of this approach failed to demonstrate outcome improvement, but did increase cesarean delivery rates.

The magnitude of risk for intrapartum fetal neurologic injury is a matter of some dispute. In 2014, the American College of Obstetricians and Gynecologists (ACOG) Task Force on Neonatal Encephalopathy concluded that 70% of these types of fetal neurologic injuries result from events that occur before the onset of labor. Examples of antepartum events that may cause fetal neurologic injury include congenital anomalies, chemical exposure, infection, and fetal thrombosis/coagulopathy. Only 4% of cases of neonatal encephalopathy result solely from intrapartum hypoxia, an incidence of approximately 1.5/1000. The Task Force criteria are consistent with clinical findings in a case series of neurologically impaired infants with intrapartum compromise. An additional case series of sentinel events (i.e., uterine rupture, cord prolapse, placental abruption, amniotic fluid embolus) during labor described a high rate of hypoxic-ischemic encephalopathy in surviving infants. Although a low percentage of neonatal encephalopathy is caused by intrapartum hypoxia, approximately 25% of fetuses may have antepartum and intrapartum risk factors for neurologic injury. Box 8.1 lists findings that suggest an acute intrapartum hypoxic-ischemic event contributed to neonatal encephalopathy.

Box 8.1

Neonatal Encephalopathy and Association with Peripartum Intrapartum Events

Definition of Neonatal Encephalopathy

Syndrome of disturbed neurologic function in the earliest days of life in an infant born at ≥ 35 weeks’ gestation

Neonatal signs consistent with an acute peripartum or intrapartum event:

1.

Apgar scores less than 5 at 5 minutes and 10 minutes of life
2.

Evidence of metabolic acidosis in umbilical cord arterial blood obtained at delivery (i.e., pH < 7.00, base deficit > 12 mmol/L)
3.

Neuroimaging evidence of acute brain injury seen on brain magnetic resonance imaging or magnetic resonance spectroscopy consistent with hypoxemia-ischemia
4.

Presence of multisystem organ failure consistent with hypoxic-ischemic encephalopathy

Type and timing of contributing factors that are consistent with an acute peripartum or intrapartum event:

1.

Sentinel hypoxic or ischemic event occurring immediately before or during labor and delivery (i.e., uterine rupture, abruption, amniotic fluid embolus)
2.

Fetal heart rate monitor patterns consistent with an acute peripartum or intrapartum event
3.

Type and timing of brain injury pattern based on imaging studies consistent with an etiology of an acute peripartum or intrapartum event
4.

No evidence of other proximal or distal factors that could be contributing events

Developmental outcome is spastic quadriplegia or dyskinetic cerebral palsy.

Modified from the American College of Obstetricians and Gynecologists. Executive summary: Neonatal encephalopathy and neurologic outcome, 2nd ed. Report of the American College of Obstetricians and Gynecologists’ Task Force on Neonatal Encephalopathy. Obstet Gynecol. 2014;123:896–901.

The ability of obstetricians to recognize and treat pregnancies at risk for hypoxia during labor is an evolving science. With the current understanding of pathophysiology and the contemporary technology used clinically, the extent to which obstetricians can prevent intrapartum injury remains unclear. Obstetricians need clear pathophysiology-based definitions of intrapartum injury. Improved monitoring technologies and standardized interpretation will enhance ascertainment of the fetus at risk. Research may result in the development of new strategies and interventions that can specifically identify and correct reversible pathophysiology.

Efforts to understand placental physiology and pathophysiology are central to efforts to support the health of the pregnant woman and her fetus, both antepartum and intrapartum. The fetus depends on the placenta for the diffusion of nutrients and for respiratory gas exchange. Many factors affect placental transfer, including concentration gradients, villus surface area, placental permeability, and placental metabolism (see Chapter 4 ). Maternal hypertensive disease, congenital anomalies, and intrauterine infection are examples of conditions that may impair placental transfer.

One of the most important determinants of placental function is uterine blood flow. A uterine contraction results in a transient decrease in uteroplacental blood flow. A placenta with borderline function before labor may be unable to adequately maintain gas exchange to prevent fetal asphyxia during labor. The healthy fetus may compensate for the effects of hypoxia during labor. The compensatory response includes (1) decreased oxygen consumption, (2) vasoconstriction of nonessential vascular beds, and (3) redistribution of blood flow to the vital organs (e.g., brain, heart, adrenal glands, placenta). Humoral responses (e.g., release of epinephrine from the adrenal medulla, release of vasopressin and endogenous opioids) may enhance fetal cardiac function during hypoxia. Prolonged or severe hypoxia overwhelms these compensatory mechanisms, resulting in fetal injury or death .

Intrapartum Fetal Assessment

Electronic Fetal Heart Rate Monitoring

There is need for a sensitive yet specific method for determination of fetal health during labor and delivery. Most contemporary methods include assessment of the FHR. The FHR can be monitored intermittently with a simple DeLee or Pinard stethoscope. Alternatively, either Doppler ultrasonography or a fetal electrocardiography (ECG) electrode can be used to monitor the FHR intermittently or continuously.

Experimental models have provided insight into the regulation of the FHR. Both neuronal and humoral factors affect the intrinsic FHR. Parasympathetic outflow by means of the vagus nerve decreases the FHR, whereas sympathetic activity increases FHR and cardiac output. Baroreceptors respond to increased blood pressure, and chemoreceptors respond to decreased Pa o ₂and increased Pa co ₂to modulate the FHR through the autonomic nervous system. Cerebral cortical activity and hypothalamic activity affect the FHR through their effects on integrative centers in the medulla oblongata ( Fig. 8.1 ). Both animal studies and clinical observations have helped establish a correlation between FHR and perinatal outcome.

An electronic monitor simultaneously records the FHR and uterine contractions. Use of an electronic monitor allows determination of the baseline rate and patterns of the FHR and their relationship to uterine contractions. External or internal techniques can assess the FHR and uterine contractions ( Fig. 8.2 ). Doppler ultrasonography detects the changes in ventricular wall motion and blood flow in major vessels during each cardiac cycle. The monitor calculates the FHR by measuring the intervals between fetal myocardial contractions. Alternatively, an ECG lead attached to the fetal scalp enables the cardiotachometer to calculate the FHR by measuring each successive R-R interval. Both external and internal methods allow continuous assessment of the FHR.

The FHR is superimposed over the uterine contraction pattern. Uterine contractions can be monitored externally with a tocodynamometer or internally with an intrauterine pressure catheter. The tocodynamometer allows determination of the approximate onset, duration, and offset of each uterine contraction. A normal pattern of uterine contractions in labor is five or less in a 10-minute period, averaged over 30 minutes; tachysystole is defined as more than five contractions in a 10-minute period. An intrauterine pressure catheter may be used to measure the relative strength, and the onset and offset, of each uterine contraction with greater precision than an external monitor. Such information may be used to distinguish among early, variable, and late FHR decelerations. Additionally, the intrauterine pressure catheter may be useful for obese parturients where the tocodynamometer lacks sensitivity. In a randomized controlled trial, internal tocodynamometry did not improve labor or neonatal outcome in a general population compared with external contraction measurements. The FDA has approved a new device (“LaborView”, OBMedical, Newberry, FL) utilizing electrohysterography, a technique that measures uterine electrical activity across the maternal wall, which may decrease the need for intrauterine pressure catheter placement.

The following features of the FHR pattern can be assessed: (1) baseline measurements, (2) variability (the extent to which the rate changes both instantaneously and over longer periods), (3) accelerations , and (4) decelerations and their association with uterine contractions.

Baseline Fetal Heart Rate

A normal baseline FHR is defined as 110 to 160 beats per minute (bpm) and is determined by assessing the mean heart rate over a 10-minute period rounded to increments of 5 bpm. In general, term fetuses have a lower baseline FHR than preterm fetuses because of greater parasympathetic nervous system activity. Laboratory studies suggest that bradycardia (caused by increased vagal activity) is the initial fetal response to acute hypoxemia. After prolonged hypoxemia, the fetus may experience tachycardia as a result of catecholamine secretion and sympathetic nervous system activity. Changes in baseline FHR may also be caused by fetal anatomic or functional heart pathology, maternal fever and/or intrauterine infection, or maternally administered medications, such as beta-adrenergic receptor agonists (e.g., terbutaline) or the anticholinergic agent atropine.

Fetal Heart Rate Variability

Fetal heart rate variability is the fluctuation in the FHR of two cycles or greater per minute. Previously, FHR variability was divided into short term (from one beat, or R wave, to the next) and long term (occurring over the course of 1 minute), but this distinction is no longer made because in clinical practice variability is visually assessed as a unit ( Fig. 8.3 ). The presence of normal FHR variability reflects the presence of normal, intact pathways from—and within—the fetal cerebral cortex, midbrain, vagus nerve, and cardiac conduction system (see Fig. 8.1 ). Variability is greatly influenced by the parasympathetic tone, by means of the vagus nerve. Maternal administration of atropine, which readily crosses the placenta, can eliminate some variability. In humans, the sympathetic nervous system appears to have a lesser role in influencing variability. Maternal administration of the beta-adrenergic receptor antagonist propranolol has little effect on FHR variability.