OBG_1106_Dildy.finalREV 10/24/06 10:05 AM Page 30 OBGMANAGEMENT Gary A. Dildy III, MD OBSTETRIC EMERGENCIES Clinical Professor, Department of Obstetrics 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 bradycardia” 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 amniotic fluid pathophysiologic mechanisms and clinical 3 FHR patterns: embolism or uterine rupture during vagi- management may differ substantially. What would nal birth 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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OBG_1106_Dildy.final 10/20/06 1:45 PM Page 33 Management of prolonged decelerations ▲ TABLE 1 Some causes of prolonged decelerations and bradycardias PROLONGED DECELERATION BRADYCARDIA Cord compression Congenital conduction abnormalities Oligohydramnios 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 hypotension by ultrasound) Hypertonic or prolonged contractions Abruptio placentae Uterine rupture Medications Cocaine ingestion Beta blockers Maternal hypoxia Maternal seizures, eclampsia Hypothermia Respiratory depression from medications Cardiopulmonary arrest Infection Amniotic fluid embolism Chorioamnionitis Endotoxemia Fetal hemorrhage Vasa previa Traumatic amniocentesis Fetal vagal reaction Rapid descent, impending birth Cervical examination Fetal scalp electrode placement Fetal blood sampling Fetal central nervous system 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 CONTINUED www.obgmanagement.com November 2006 • OBG MANAGEMENT 33 OBG_1106_Dildy.finalREV 10/24/06 10:05 AM Page 37 Management of ▲ prolonged decelerations 75 years of age. In women greater than 75, the increased risk of non-fatal stroke and invasive breast cancer observed in the estrogen-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 gestations 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