Clinical Review

Management of prolonged decelerations

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References

The findings:

TABLE 2

Neonatal outcomes associated with variability and recovery of FHR patterns after prolonged deceleration

UMBILICAL ARTERYGROUP 1 V+ R+ (N=128)GROUP 2 V+ R- (N=40)GROUP 3 V- R+ (N=9)GROUP 4 V- R- (N=9)P VALUE
pH (mean±SD)7.17±0.097.13±0.157.11±0.116.83±0.16<.001
Base deficit (mean±SD)-6.5±3.9-7.2±5.1-10±4-20±6<.001
pH <7.0 (%)2184478<.001
pH <7.1 (%)22335689<.001
Base deficit <16 (%)181178<.001
Base deficit <12 (%)5132289<.001
V=variability
R=recovery
SOURCE: Williams and Galerneau9

Acid–base changes likely begin within minutes of cord compression

Zilianti and colleagues10 evaluated 29 fetuses with normal FHR patterns during labor with FHR deceleration during the expulsion phase of delivery. When the FHR deceleration was prolonged (>120 seconds), umbilical artery pH significantly decreased (7.19 vs 7.27), umbilical vein pH remained unchanged (7.32), and the umbilical venous–arterial pH difference was significantly increased (0.13 vs 0.05). Thus, acid–base changes likely begin within minutes of cord compression.

The correlation between acidemia and loss of variability

In their review of 43 vacuum extractions, Gull and colleagues22 found that 27 infants were delivered for “end-stage bradycardia” (abrupt persistent decrease in FHR to less than 100 bpm for more than 2 minutes, or repeated deceleration more than 60 bpm below baseline with poor recovery), and 16 were delivered electively (controls). Umbilical-cord base deficit was greater in the newborns with bradycardia than in controls, and the length of time FHR variability was lost correlated with the degree of base deficit. Acidemic fetuses lost FHR variability during the bradycardia for more than 4 minutes, or started to lose FHR variability less than 3 minutes from the beginning of the bradycardia.

What is optimal interval between deceleration and delivery?

In a series of 106 cases of uterine rupture during VBAC, Leung et al11 found significant neonatal morbidity when 18 minutes or more lapsed between the onset of the prolonged deceleration and delivery.

First, remain calm when decelerations occur

Freeman and colleagues12 advocate staying calm and avoiding overreaction, because many cases will resolve spontaneously. Nonetheless, prolonged decelerations should prompt the physician to:

TABLE 3

6 pearls for managing prolonged decelerations

GOALPEARL
1Reduce aorto-caval and/or cord compressionChange patient positioning
2Restore intravascular volumeAdminister intravenous fluid bolus
3Reduce uterine activityDiscontinue oxytocin drip and give tocolytic therapy (terbutaline)
4Enhance oxygen delivery to fetusGive supplemental oxygen
5Resolve hypotensionAdminister vasopressor therapy (ephedrine)
6Resolve oligohydramnios and cord compressionPerform transcervical amnioinfusion

TABLE 4

Stepwise management of prolonged decelerations

Examine the cervix
Check for umbilical cord prolapse
Check progress of dilation and descent
Place internal monitors, if indicated
Determine probable cause
Start therapies
Prepare for intervention by operative delivery
Intravenous access
Blood type and screen
Indwelling urinary catheter
Obtain consents for operative vaginal delivery and cesarean delivery
Notify appropriate personnel (eg, anesthesiology, pediatrics)
Deliver
If fetal condition is nonreassuring despite therapies
If prolonged decelerations recur and spontaneous delivery is remote (cases must be individualized)

Consider amnioinfusion when cord compression is suspected

Many cases of prolonged decelerations are secondary to cord compression resulting from oligohydramnios. Miyazaki13 showed that saline amnioinfusion helped correct the FHR problem in most cases of repetitive variable decelerations (19 of 28) and prolonged decelerations (12 of 14 cases).

Several randomized clinical trials analyzed in a recent Cochrane Review14 suggest that amnioinfusion for cord compression reduces the occurrence of variable FHR decelerations and the need for cesarean section; this applies to settings in which nonreassuring FHR patterns were not further assessed by fetal blood sampling, which is reflective of practice in most US labor units.

The recent ACOG practice bulletin on intrapartum monitoring4 advocates amnioinfusion for recurrent variable FHR decelerations, but does not address prolonged decelerations specifically.

Although most data on amnioinfusion address treatment of recurrent variable FHR decelerations, it also seems reasonable to consider this option for prolonged decelerations when oligohydramnios is suspected.12

Other possible causes of prolonged decelerations

Vasa previa. A sudden prolonged deceleration following rupture of membranes with concomitant vaginal bleeding should prompt the physician to consider the possibility of a disrupted velamentous cord insertion (vasa previa), which can lead to rapid fetal exsanguination.15

Acute profound maternal hypoxemia may lead to a first prolonged FHR deceleration, often preceded by increased uterine tone, as described in both eclampsia16 and amniotic fluid embolism.17 With eclampsia, the prolonged deceleration is reversible; treatment and expectant management will allow for fetal recovery after the seizure abates.

When acute amniotic fluid embolism leads to profound cardiovascular collapse, prompt perimortem cesarean delivery may be required within minutes if CPR does not restore normal maternal cardiopulmonary function and recovery of FHR.

When is scalp stimulation helpful?

Stimulation of the fetal scalp is an effective technique for assessing fetal status during periods of nonreassuring FHR patterns.18 However, the technique is intended to be performed during periods of FHR baseline and is sometimes misapplied during prolonged decelerations. Scalp stimulation during a prolonged deceleration would not likely provide valid information or change clinical management and could in theory exacerbate fetal compromise if additional parasympathetic tone were elicited.

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