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OBGMANAGEMENT

Gary A. Dildy III, MD OBSTETRIC EMERGENCIES Clinical Professor, Department of and Gynecology, Management of Louisiana State University Health Sciences Center New Orleans prolonged decelerations

Director of Site Analysis HCA Perinatal Quality Assurance Some are benign, some are pathologic but reversible, Nashville, Tenn and others are the most feared complications in obstetrics Staff Perinatologist Maternal-Fetal Medicine St. Mark’s Hospital prolonged deceleration may signal ed prolonged decelerations is based on bed- Salt Lake City, Utah danger—or reflect a perfectly nor- side clinical judgment, which inevitably will A mal fetal response to maternal sometimes be imperfect given the unpre- pelvic examination.® BecauseDowden of the Healthwide dictability Media of these decelerations.” range of possibilities, this fetal heart rate pattern justifies close attention. For exam- “Fetal ” and “prolonged ple,Copyright repetitive Forprolonged personal decelerations use may onlydeceleration” are distinct entities indicate cord compression from oligohy- In general parlance, we often use the terms dramnios. Even more troubling, a pro- “fetal bradycardia” and “prolonged decel- longed deceleration may occur for the first eration” loosely. In practice, we must dif- IN THIS ARTICLE time during the evolution of a profound ferentiate these entities because underlying catastrophe, such as pathophysiologic mechanisms and clinical 3 FHR patterns: or during vagi- management may differ substantially. What would nal after cesarean delivery (VBAC). The problem: Since the introduction In some circumstances, a prolonged decel- of electronic fetal monitoring (EFM) in you do? eration may be the terminus of a progres- the 1960s, numerous descriptions of FHR ❙ Complete heart sion of nonreassuring fetal heart rate patterns have been published, each slight- block (FHR) changes, and becomes the immedi- ly different from the others. The result: ate precursor to fetal death (TABLE 1).1 confusing nomenclature, miscommunica- ❙ Prolonged When FHR patterns exhibit these tion among clinicians, and stymied deceleration aberrations, we rightly worry about fetal research efforts. well-being and the possible need for oper- To standardize definitions of intra- during pelvic exam ative intervention. Unfortunately, the partum FHR patterns so that the effective- ❙ Uterine rupture degree of fetal compromise is difficult to ness of EFM could be better assessed in Page 38 predict and depends on preexisting fetal observational studies and clinical trials, the condition, physiologic reserve, degree and National Institute of Child Health and 6 pearls for duration of the insult, and other variables. Human Development organized a work- shop.3 Its recommendations were subse- managing prolonged Ultimately, a judgment call quently adopted by the American College decelerations The 22nd edition of Williams Obstetrics2 of Obstetricians and Gynecologists Page 45 summarizes the clinical challenges involved (ACOG).4 Among the definitions: in the management of prolonged decelera- • Bradycardia: a baseline FHR of less tions during labor: “Management of isolat- than 110 beats per minute.

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Management of prolonged decelerations ▲

TABLE 1 Some causes of prolonged decelerations and

PROLONGED DECELERATION BRADYCARDIA Cord compression Congenital conduction abnormalities Complete heart block Cord prolapse Long QT syndrome Congenital heart defects Uteroplacental insufficiency Tachyarrhythmia (Fetal tachyarrhythmia may Anesthesia (paracervical, spinal, epidural) produce an EFM tracing that appears to be Maternal valsalva a bradycardia and can only be distinguished Maternal supine by ultrasound) Hypertonic or prolonged contractions Abruptio placentae Uterine rupture Medications Cocaine ingestion Beta blockers Maternal Maternal seizures, Hypothermia Respiratory depression from medications Cardiopulmonary arrest Endotoxemia Fetal hemorrhage Vasa previa Traumatic Fetal vagal reaction Rapid descent, impending birth Cervical examination Fetal scalp electrode placement Fetal sampling Fetal central anomalies Idiopathic (cord compression?) FAST TRACK Fetal bradycardias • Prolonged deceleration: a visually tion, resolving after rotation of the fetal apparent decrease of 15 or more beats vertex and associated with normal and prolonged per minute below the baseline. This neonatal outcome.5,6 decelerations decrease lasts at least 2 minutes but less are 2 distinct than 10 minutes from onset to the entities; the first return to baseline (≥10 minutes is con- ❚ Similar decelerations can sidered a baseline change). usually does not Differentiation between the 2 entities is critical reflect different events warrant immediate because, in many cases, bradycardias are The exact depth and duration of a pro- intervention chronic patterns that may not be associat- longed deceleration leading to fetal com- ed with immediate fetal compromise and promise and requiring prompt delivery is do not require immediate intervention. For difficult to define, although some observa- example, a fetal bradycardia due to con- tions warrant consideration. Experiments genital heart block would not benefit from with fetal lambs show that the decelera- immediate delivery, especially prior to tion in response to umbilical vein occlu- term. sion is associated with a fall in fetal blood “Moderate fetal bradycardia,” pressure, whereas deceleration in response defined as a baseline of 100 to 119 bpm, to umbilical artery occlusion is associated was reported in 1.8% of 1,386 continu- with a rise in fetal blood pressure. This ously monitored patients and is attrib- reflex can be abolished by vagotomy, but uted to relative cephalopelvic dispropor- will eventually recur due to anoxia.7

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Management of ▲ prolonged decelerations 75 years of age. In women greater than 75, the increased risk of non-fatal stroke and invasive cancer observed in the -plus-progestin combination group compared to the placebo group was 75 vs. 24 per 10,000 women-years and 52 vs. 12 per 10,000 women years, respectively. In the estrogen-plus-progestin WHIMS substudy, a population of 4,532 postmenopausal women, aged 65 to 79 years, was randomized to CE/MPA (0.625 mg/2.5 mg daily) or placebo. In the estrogen-plus-progestin group, after an average follow-up of four years, the relative risk (CE/MPA vs. placebo) of probable dementia was 2.05 (95% CI 1.21- Vital clue: What happened before 3.48). The absolute risk of developing probable dementia with CE/MPA was 45 vs. 22 cases per 10,000 women-years with placebo. the prolonged deceleration? Seventy-nine percent of the cases of probable dementia occurred in women that were older than 70 for the CE group,and 82 percent of the cases of probable dementia occurred In clinical practice, it is important to in women who were older than 70 in the CE/MPA group.The most common classification of probable dementia in both the treatment groups was Alzheimer’s disease. appreciate characteristics of the FHR pat- When data from the two populations were pooled as planned in the WHIMS protocol, the reported overall relative risk for probable dementia was 1.76 (95% CI 1.19-2.60). tern preceding the prolonged deceleration.8 Since both substudies were conducted in women aged 65 to 79 years, it is unknown whether these findings apply to younger postmenopausal women. (See BOXED Williams and Galerneau9 correlated baseline WARNINGS and WARNINGS, Dementia.) With respect to efficacy in the approved indications, there have not been sufficient numbers of geriatric patients involved in studies utilizing Premarin to determine whether FHR variability and duration of prolonged those over 65 years of age differ from younger subjects in their response to Premarin. ADVERSE REACTIONS decelerations with neonatal acid–base status See BOXED WARNINGS, WARNINGS, and PRECAUTIONS. Because clinical trials are conducted under widely varying conditions, adverse reaction in 186 term with an identified rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.The adverse prolonged deceleration within 30 minutes reaction information from clinical trials does, however, provide a basis for identifying the adverse events that appear to be related to drug use and for approximating rates. of delivery. Patients were divided into 4 During the first year of a 2-year clinical trial with 2,333 postmenopausal women between 40 and 65 years of age (88% Caucasian), 1,012 women were treated with groups, based on FHR variability and recov- conjugated estrogens and 332 were treated with placebo. Table 6 summarizes adverse events that occurred at a rate of ≥ 5%. ery of the FHR baseline (TABLE 2). TABLE 6. NUMBER (%) OF PATIENTS REPORTING ≥ 5% TREATMENT EMERGENT ADVERSE EVENTS The findings: — Conjugated Estrogens Treatment Group — Body System 0.625 mg 0.45 mg 0.3mg Placebo • Lowest cord pH was associated with Adverse event (n = 348) (n = 338) (n = 326) (n = 332) decreased variability without recovery Any adverse event 323 (93%) 305 (90%) 292 (90%) 281 (85%) Body as a Whole 56 (16%) 50 (15%) 54 (17%) 37 (11%) of the FHR Accidental 21 (6%) 41 (12%) 20 (6%) 29 (9%) Asthenia 25 (7%) 23 (7%) 25 (8%) 16 (5%) • Neonatal acidemia was most strongly Back pain 49 (14%) 43 (13%) 43 (13%) 39 (12%) Flu syndrome 37 (11%) 38 (11%) 33 (10%) 35 (11%) correlated with decreased variability Headache 90 (26%) 109 (32%) 96 (29%) 93 (28%) Infection 61 (18%) 75 (22%) 74 (23%) 74 (22%) before the prolonged deceleration Pain 58 (17%) 61 (18%) 66 (20%) 61 (18%) Digestive System Diarrhea 21 (6%) 25 (7%) 19 (6%) 21 (6%) Dyspepsia 33 (9%) 32 (9%) 36 (11%) 46 (14%) Acid–base changes likely begin Flatulence 24 (7%) 23 (7%) 18 (6%) 9 (3%) Nausea 32 (9%) 21 (6%) 21 (6%) 30 (9%) within minutes of cord compression Musculoskeletal System Arthralgia 47 (14%) 42 (12%) 22 (7%) 39 (12%) Zilianti and colleagues10 evaluated 29 Leg cramps 19 (5%) 23 (7%) 11 (3%) 7 (2%) Myalgia 18 (5%) 18 (5%) 29 (9%) 25 (8%) Nervous System with normal FHR patterns during Depression 25 (7%) 27 (8%) 17 (5%) 22 (7%) Dizziness 19 (5%) 20 (6%) 12 (4%) 17 (5%) labor with FHR deceleration during the Insomnia 21 (6%) 25 (7%) 24 (7%) 33 (10%) Nervousness 12 (3%) 17 (5%) 6 (2%) 7 (2%) expulsion phase of delivery. When the Respiratory System Cough increased 13 (4%) 22 (7%) 14 (4%) 14 (4%) FHR deceleration was prolonged (>120 Pharyngitis 35 (10%) 35 (10%) 40 (12%) 38 (11%) Rhinitis 21 (6%) 30 (9%) 31 (10%) 42 (13%) seconds), umbilical artery pH significantly Sinusitis 22 (6%) 36 (11%) 24 (7%) 24 (7%) Upper respiratory infection 42 (12%) 34 (10%) 28 (9%) 35 (11%) decreased (7.19 vs 7.27), umbilical vein Skin and Appendages Pruritus 14 (4%) 17 (5%) 16 (5%) 7 (2%) pH remained unchanged (7.32), and the Urogenital System 38 (11%) 41 (12%) 24 (7%) 29 (9%) umbilical venous–arterial pH difference Leukorrhea 18 (5%) 22 (7%) 13 (4%) 9 (3%) Vaginal hemorrhage 47 (14%) 14 (4%) 7 (2%) 0 was significantly increased (0.13 vs 0.05). Vaginal moniliasis 20 (6%) 18 (5%) 17 (5%) 6 (2%) Vaginitis 24 (7%) 20 (6%) 16 (5%) 4 (1%) Thus, acid–base changes likely begin with- The following additional adverse reactions have been reported with estrogen and/or progestin therapy: in minutes of cord compression. 1. Genitourinary system Changes in vaginal pattern and abnormal withdrawal bleeding or flow; breakthrough bleeding, spotting, ; increase in size of uterine leiomyomata; vaginitis, including vaginal candidiasis; change in amount of cervical secretion; change in The correlation between acidemia cervical ectropion; ovarian cancer; endometrial hyperplasia; endometrial cancer. 2. and loss of variability Tenderness, enlargement, pain, discharge, , fibrocystic breast changes; breast cancer. In their review of 43 vacuum extractions, 3. Cardiovascular Deep and superficial venous thrombosis, , thrombophlebitis, Gull and colleagues22 found that 27 myocardial infarction, stroke, increase in blood pressure 4. Gastrointestinal were delivered for “end-stage bradycar- Nausea, vomiting; abdominal cramps, bloating; cholestatic jaundice; increased incidence of gallbladder disease; pancreatitis; enlargement of hepatic hemangiomas. dia” (abrupt persistent decrease in FHR to 5. Skin Chloasma or that may persist when drug is discontinued; erythema multiforme; less than 100 bpm for more than 2 min- erythema nodosum; hemorrhagic eruption; loss of scalp hair; hirsutism; pruritus, rash. 6. Eyes utes, or repeated deceleration more than Retinal vascular thrombosis, intolerance to contact lenses 7. Central Nervous System 60 bpm below baseline with poor recov- Headache, migraine, dizziness, mental depression, chorea, nervousness, mood disturbances, irritability, exacerbation of epilepsy, dementia. ery), and 16 were delivered electively (con- 8. Miscellaneous Increase or decrease in weight; reduced tolerance; aggravation of trols). Umbilical-cord base deficit was porphyria; ; arthralgias; leg cramps; changes in libido; urticaria, angioedema, anaphylactoid/anaphylactic reactions; hypocalcemia; exacerbation of asthma; greater in the newborns with bradycardia increased triglycerides. OVERDOSAGE than in controls, and the length of time Serious ill effects have not been reported following acute ingestion of large doses of estrogen-containing drug products by young children. Overdosage of estrogen may FHR variability was lost correlated with cause nausea and vomiting, and withdrawal bleeding may occur in females. This brief summary is based on PREMARIN® (conjugated estrogens tablets, USP) the degree of base deficit. Acidemic fetuses Prescribing Information W10405C017 ET01, revised April 2006. CONTINUED

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3 fetal heart rate patterns: What would you do?

Complete heart block Dilemma Fetal bradycardia due to congenital complete heart block secondary to anti-SS- A/Ro and anti-SS-B/La antibodies. The fetal ventricular rate is fixed at 60 bpm

Management At 30 weeks’ , with no sonographic evidence of heart failure and a score of 8/8, expectant management is indicated

Prolonged deceleration during pelvic exam Dilemma Prolonged deceleration during pelvic examination in an uncomplicated term . Note that fetal heart rate (FHR) variability was maintained during recovery of the FHR baseline

Outcome Uneventful spontaneous vaginal delivery

Uterine rupture Dilemma Prolonged deceleration due to uterine rupture during trial of labor after cesarean. Repetitive variable decelerations preceded the prolonged deceleration. FHR variability was lost after several minutes

Outcome Emergency cesarean

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TABLE 2 Neonatal outcomes associated with variability and recovery of FHR patterns after prolonged deceleration

UMBILICAL ARTERY GROUP 1 GROUP 2 GROUP 3 GROUP 4 V+ R+ V+ R- V- R+ V- R- (N = 128) (N = 40) (N = 9) (N = 9) P VALUE pH (mean ± SD) 7.17 ± 0.0 9 7.13 ± 0.15 7.11 ± 0.11 6.8 3 ± 0.16 < .0 01 Base deficit -6.5 ±3.9 -7.2 ±5.1 -10 ±4 -20 ±6 <.001 (mean ± SD) pH <7.0 (%) 218 4478<.001 pH <7.1 (%) 22 33 56 89 <.001 Base deficit <16 (%) 18 1178<.001 Base deficit <12 (%) 513 2289<.001

V = variability R = recovery SOURCE: Williams and Galerneau9

lost FHR variability during the bradycar- from oligohydramnios. Miyazaki13 showed dia for more than 4 minutes, or started to that saline helped correct lose FHR variability less than 3 minutes the FHR problem in most cases of repeti- from the beginning of the bradycardia. tive variable decelerations (19 of 28) and prolonged decelerations (12 of 14 cases). What is optimal interval between Several randomized clinical trials ana- deceleration and delivery? lyzed in a recent Cochrane Review14 sug- In a series of 106 cases of uterine rupture gest that amnioinfusion for cord compres- during VBAC, Leung et al11 found signifi- sion reduces the occurrence of variable cant neonatal morbidity when 18 minutes FHR decelerations and the need for cesare- FAST TRACK or more lapsed between the onset of the an section; this applies to settings in which Amnioinfusion for prolonged deceleration and delivery. nonreassuring FHR patterns were not fur- ther assessed by fetal blood sampling, cord compression which is reflective of practice in most US reduces variable labor units. ❚ First, remain calm when FHR decelerations The recent ACOG practice bulletin on decelerations occur 4 and the need for intrapartum monitoring advocates Freeman and colleagues12 advocate staying amnioinfusion for recurrent variable FHR cesarean section calm and avoiding overreaction, because decelerations, but does not address pro- many cases will resolve spontaneously. longed decelerations specifically. Nonetheless, prolonged decelerations Although most data on amnioinfusion should prompt the physician to: address treatment of recurrent variable • consider the underlying pathophysi- FHR decelerations, it also seems reason- ology and implement corrective able to consider this option for prolonged interventions (TABLE 3) decelerations when oligohydramnios is • further assess fetal condition suspected.12 • prepare for the possibility of immediate delivery (TABLE 4) Other possible causes of prolonged decelerations Consider amnioinfusion when cord Vasa previa. A sudden prolonged decelera- compression is suspected tion following with Many cases of prolonged decelerations are concomitant should secondary to cord compression resulting prompt the physician to consider the pos-

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Management of prolonged decelerations ▲

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 drip and give therapy (terbutaline) 4 Enhance oxygen delivery to Give supplemental oxygen 5 Resolve hypotension Administer vasopressor therapy (ephedrine) 6 Resolve oligohydramnios and cord compression Perform transcervical amnioinfusion

sibility of a disrupted velamentous cord longed deceleration is an absolute con- insertion (vasa previa), which can lead to traindication to its use.21 rapid fetal exsanguination.15 Acute profound maternal hypoxemia may Summary lead to a first prolonged FHR decelera- Overall, in managing a delivery marked by tion, often preceded by increased uterine prolonged decelerations, we should strive tone, as described in both eclampsia16 and to minimize maternal–fetal complications amniotic fluid embolism.17 With eclamp- by carefully assessing the clinical situation, sia, the prolonged deceleration is correcting reversible problems, and reversible; treatment and expectant man- preparing for expeditious delivery if the agement will allow for fetal recovery after fetal condition is of sufficient concern that the seizure abates. further expectant management is unlikely When acute amniotic fluid embolism to allow for safe spontaneous delivery. leads to profound cardiovascular collapse, Still, “...bedside judgment inevitably will prompt perimortem cesarean delivery may sometimes be imperfect given the unpre- be required within minutes if CPR does dictability of these decelerations.”2 ■ not restore normal maternal cardiopul- FAST TRACK monary function and recovery of FHR. REFERENCES 1. Cetrulo CL, Schifrin BS. Fetal heart rate patterns preceding Fetal scalp When is scalp stimulation helpful? death in utero. Obstet Gynecol. 1976;48:521–527. stimulation to 2. Cunningham FG, Leveno KJ, Bloom SL, et al. Williams Stimulation of the fetal scalp is an effec- Obstetrics. 22nd ed. New York: McGraw-Hill; 2005. assess fetal status tive technique for assessing fetal status 3. Electronic fetal heart rate monitoring: research guidelines should be done during periods of nonreassuring FHR for interpretation. National Institute of Child Health and during periods patterns.18 However, the technique is Human Development Research Planning Workshop. Am J Obstet Gynecol. 1997;177:1385–1390. intended to be performed during periods of FHR baseline 4. Intrapartum fetal heart rate monitoring. ACOG Practice of FHR baseline and is sometimes misap- Bulletin #70. American College of Obstetricians and plied during prolonged decelerations. Gynecologists. Obstet Gynecol. 2005;106:1453–1461. Scalp stimulation during a prolonged 5. Young BK, Weinstein HM. Moderate fetal bradycardia. Am J deceleration would not likely provide Obstet Gynecol. 1976;126:271–275. valid information or change clinical man- 6. Young BK, Katz M, et al. Fetal blood and tissue pH with mod- erate bradycardia. Am J Obstet Gynecol. 1979;135:45–47. agement and could in theory exacerbate 7. Reynolds SR. Bradycardia in the lamb fetus in response to fetal compromise if additional parasym- circulatory distress. Am J Physiol. 1954;176:169–174. pathetic tone were elicited. 8. Langer O, Sonnendecker EW.Characteristics and manage- ment of intrapartum prolonged fetal bradycardia. Br J Avoid fetal pulse oximetry Obstet Gynaecol. 1982;89:904–912. Although fetal pulse oximetry is FDA- 9. Williams KP, Galerneau F. Fetal heart rate parameters pre- dictive of neonatal outcome in the presence of a prolonged approved and commercially available in deceleration. Obstet Gynecol. 2002;100:951–954. the United States, and may be well suited 10. Zilianti M, Segura CL, et al. Studies on fetal bradycardia for monitoring fetal arrhythmias,19,20 a pro- during birth process. II. Obstet Gynecol. 1973;42:840–843.

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TABLE 4 variable or prolonged decelerations. A preliminary report. Stepwise management of prolonged decelerations Am J Obstet Gynecol. 1983;146:670–678. 14. Hofmeyr GJ. Amnioinfusion for compression in labour. Cochrane Database Syst Rev. 2000:CD000013. Examine the 15. Gabbe SG, Nelson LM, Paul RH. Fetal heart rate response • Check for to acute hemorrhage. Obstet Gynecol. 1977;49:247–251. • Check progress of dilation and descent 16. Paul RH, Koh KS, Bernstein SG. Changes in fetal heart rate- • Place internal monitors, if indicated patterns associated with eclampsia. Am J Obstet Gynecol. 1978;130:165–169. Determine probable cause 17. Clark SL, Hankins GD, Dudley DA, Dildy GA, Porter TF. Start therapies Amniotic fluid embolism: analysis of the national registry. Am J Obstet Gynecol. 1995;172:1158–1167; discussion Prepare for intervention by operative delivery 1167–1169. • Intravenous access 18. Clark SL, Gimovsky ML, Miller FC. The scalp stimulation • Blood type and screen test: a clinical alternative to fetal scalp blood sampling. Am J Obstet Gynecol. 1984;148:274–277. • Indwelling urinary catheter 19. Dildy GA, Loucks CA, Clark SL. Intrapartum fetal pulse • Obtain consents for operative vaginal delivery and cesarean delivery oximetry in the presence of fetal cardiac arrhythmia. Am J • Notify appropriate personnel (eg, anesthesiology, pediatrics) Obstet Gynecol. 1993;169:1609–1611. Deliver 20. van den Berg PP, Nijland R, van den Brand SF, Jongsma HW, Nijhuis JG. Intrapartum fetal surveillance of congenital • If fetal condition is nonreassuring despite therapies heart block with pulse oximetry. Obstet Gynecol. • If prolonged decelerations recur and spontaneous delivery is 1994;84:683–686. remote (cases must be individualized) 21. Garite TJ, Dildy GA, McNamara H, et al. A multicenter con- trolled trial of fetal pulse oximetry in the intrapartum man- agement of nonreassuring fetal heart rate patterns. Am J 11. Leung AS, Leung EK, Paul RH. Uterine rupture after previ- Obstet Gynecol. 2000;183:1049–1058. ous cesarean delivery: maternal and fetal consequences. 22. Gull I, Jaffa AJ, Oren M, Grisaru D, Peyser MR, Lessing JB. Am J Obstet Gynecol. 1993;169:945–950. Acid accumulation during end-stage bradycardia in term 12. Freeman RK, Garite TG, Nageotte MP. Fetal Heart Rate fetuses: how long is too long? Br J Obstet Gynaecol. Monitoring. Philadelphia: Lippincott Williams & Wilkins; 2003. 1996;103:1096–1101. 13. Miyazaki FS, Taylor NA. Saline amnioinfusion for relief of The author reports no financial affiliations relevant to this article.

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