Clinical Review

Management of prolonged decelerations

OBG Manag. 2006 November;18(11):30-45

References

1. Cetrulo CL, Schifrin BS. Fetal heart rate patterns preceding death in utero. Obstet Gynecol. 1976;48:521-527.

2. Cunningham FG, Leveno KJ, Bloom SL, et al. Williams Obstetrics. 22nd ed. New York: McGraw-Hill; 2005.

3. Electronic fetal heart rate monitoring: research guidelines for interpretation. National Institute of Child Health and Human Development Research Planning Workshop. Am J Obstet Gynecol. 1997;177:1385-1390.

4. Intrapartum fetal heart rate monitoring. ACOG Practice Bulletin #70. American College of Obstetricians and Gynecologists. Obstet Gynecol. 2005;106:1453-1461.

5. Young BK, Weinstein HM. Moderate fetal bradycardia. Am J Obstet Gynecol. 1976;126:271-275.

6. Young BK, Katz M, et al. Fetal blood and tissue pH with moderate bradycardia. Am J Obstet Gynecol. 1979;135:45-47.

7. Reynolds SR. Bradycardia in the lamb fetus in response to circulatory distress. Am J Physiol. 1954;176:169-174.

8. Langer O, Sonnendecker EW. Characteristics and management of intrapartum prolonged fetal bradycardia. Br J Obstet Gynaecol. 1982;89:904-912.

9. Williams KP, Galerneau F. Fetal heart rate parameters predictive of neonatal outcome in the presence of a prolonged deceleration. Obstet Gynecol. 2002;100:951-954.

10. Zilianti M, Segura CL, et al. Studies on fetal bradycardia during birth process. II. Obstet Gynecol. 1973;42:840-843.

11. Leung AS, Leung EK, Paul RH. Uterine rupture after previous cesarean delivery: maternal and fetal consequences. Am J Obstet Gynecol. 1993;169:945-950.

12. Freeman RK, Garite TG, Nageotte MP. Fetal Heart Rate Monitoring. Philadelphia: Lippincott Williams & Wilkins; 2003.

13. Miyazaki FS, Taylor NA. Saline amnioinfusion for relief of variable or prolonged decelerations. A preliminary report. Am J Obstet Gynecol. 1983;146:670-678.

14. Hofmeyr GJ. Amnioinfusion for umbilical cord compression in labour. Cochrane Database Syst Rev. 2000;CD000013.-

15. Gabbe SG, Nelson LM, Paul RH. Fetal heart rate response to acute hemorrhage. Obstet Gynecol. 1977;49:247-251.

16. Paul RH, Koh KS, Bernstein SG. Changes in fetal heart rateuterine contraction patterns associated with eclampsia. Am J Obstet Gynecol. 1978;130:165-169.

17. Clark SL, Hankins GD, Dudley DA, Dildy GA, Porter TF. Amniotic fluid embolism: analysis of the national registry. Am J Obstet Gynecol. 1995;172:1158-1167;discussion 1167-1169.

18. Clark SL, Gimovsky ML, Miller FC. The scalp stimulation test: a clinical alternative to fetal scalp blood sampling. Am J Obstet Gynecol. 1984;148:274-277.

19. Dildy GA, Loucks CA, Clark SL. Intrapartum fetal pulse oximetry in the presence of fetal cardiac arrhythmia. Am J Obstet Gynecol. 1993;169:1609-1611.

20. van den Berg PP, Nijland R, van den Brand SF, Jongsma HW, Nijhuis JG. Intrapartum fetal surveillance of congenital heart block with pulse oximetry. Obstet Gynecol. 1994;84:683-686.

21. Garite TJ, Dildy GA, McNamara H, et al. A multicenter controlled trial of fetal pulse oximetry in the intrapartum management of nonreassuring fetal heart rate patterns. Am J Obstet Gynecol. 2000;183:1049-1058.

22. Gull I, Jaffa AJ, Oren M, Grisaru D, Peyser MR, Lessing JB. Acid accumulation during end-stage bradycardia in term fetuses: how long is too long? Br J Obstet Gynaecol. 1996;103:1096-1101.

The findings:

TABLE 2

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

UMBILICAL ARTERY	GROUP 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±0.09	7.13±0.15	7.11±0.11	6.83±0.16	<.001
Base deficit (mean±SD)	-6.5±3.9	-7.2±5.1	-10±4	-20±6	<.001
pH <7.0 (%)	2	18	44	78	<.001
pH <7.1 (%)	22	33	56	89	<.001
Base deficit <16 (%)	1	8	11	78	<.001
Base deficit <12 (%)	5	13	22	89	<.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

	GOAL	PEARL
1	Reduce aorto-caval and/or cord compression	Change patient positioning
2	Restore intravascular volume	Administer intravenous fluid bolus
3	Reduce uterine activity	Discontinue oxytocin drip and give tocolytic therapy (terbutaline)
4	Enhance oxygen delivery to fetus	Give supplemental oxygen
5	Resolve hypotension	Administer vasopressor therapy (ephedrine)
6	Resolve oligohydramnios and cord compression	Perform 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.