Maternal Hypotension and Tachysystole Following Neuraxial Anesthesia: Effect on Fetus in Labor
2021; American Academy of Pediatrics; Volume: 22; Issue: 9 Linguagem: Inglês
10.1542/neo.22-9-e627
ISSN1526-9906
AutoresNicole Massad, Desiree Fiorentino, Diana Wolfe,
Tópico(s)Airway Management and Intubation Techniques
ResumoElectronic fetal monitoring (EFM) is a popular technology used to establish fetal well-being. Despite its widespread use, the terminology used to describe patterns seen on the monitor has not been consistent until recently. In 1997, the National Institute of Child Health and Human Development (NICHD) Research Planning Workshop published guidelines for interpretation of fetal tracings. This publication was the culmination of 2 years of work by a panel of experts in the field of fetal monitoring and was endorsed in 2005 by both the American College of Obstetricians and Gynecologists (ACOG) and the Association of Women’s Health, Obstetric and Neonatal Nurses (AWHONN). In 2008, ACOG, NICHD, and the Society for Maternal-Fetal Medicine reviewed and updated the definitions for fetal heart rate (FHR) patterns, interpretation, and research recommendations. Following is a summary of the terminology definitions and assumptions found in the 2008 NICHD workshop report. Normal arterial umbilical cord gas values and indications of acidosis are defined in the Table.A 3-tier FHR Interpretation system has been recommended as follows: Data from Macones GA, Hankins GDV, Spong CY, Hauth J, Moore T. The 2008 National Institute of Child Health and Human Development workshop report on electronic fetal monitoring. Obstet Gynecocol. 2008;112:661-666 and American College of Obstetricians and Gynecologists. Intrapartum fetal heart rate monitoring: nomenclature, interpretation, and general management principles. ACOG Practice Bulletin No. 106. Washington, DC: American College of Obstetricians and Gynecologists; 2009.We encourage readers to examine each strip in the case presentation and make a personal interpretation of the findings before advancing to the expert interpretation provided.A 40-year-old gravida 4, para 2-0-1-2 woman with type 2 diabetes mellitus presented at 39 0/7 weeks’ gestation for scheduled induction of labor. Her antenatal course and medical history were significant for type 2 diabetes mellitus managed with insulin. Her insulin dose was titrated throughout the pregnancy in response to fasting and 2-hour postprandial glucose levels. She had tight glycemic control with a hemoglobin A1c of 5.9% at the onset of pregnancy. She had 2 prior uncomplicated spontaneous vaginal deliveries. In the third trimester, she underwent antenatal surveillance with nonstress tests and biophysical profiles along with serial growth scans. Her most recent ultrasonographic estimate of fetal weight at 36 weeks’ gestation was in the 60th percentile.On arrival at the labor department, the patient was comfortable, with intact membranes and irregular contractions every 6 to 10 minutes on the tocometer. On initial examination, her cervix was 1 to 2 cm dilated, 70% effaced, and at −3 station. She was normotensive and euglycemic. The FHR tracing is shown in Fig 1.Findings in Fig 1 were as follows: The patient requested neuraxial anesthesia before the start of her induction and had an uncomplicated combined spinal-epidural (CSE) placement. She remained normotensive. Shortly after CSE placement, she experienced uterine tachysystole associated with prolonged deceleration in the FHR (Fig 2).Findings in Fig 2 were as follows: The patient was placed in the hands-knees position and the tocolytic terbutaline was given. Her blood pressure was normal at 126/62 mm Hg. Repeat cervical examination demonstrated spontaneous cervical change to 4-cm dilation, 70% effacement, and −3 station. Penicillin was started for group B Streptococcus prophylaxis. The FHR tracing subsequently recovered to category I (Fig 3).Findings in Fig 3 were as follows: Given the resolution of the fetal deceleration and spontaneous cervical change, expectant management was advised. After 2 hours of a category I tracing, the patient again had prolonged deceleration in the setting of uterine tachysystole (Fig 4).Findings in Fig 4 were as follows: The FHR recovered to baseline with repositioning. The cervix was 5-cm dilated, 80% effaced, and at −3 station without evidence of cord prolapse. There was no vaginal bleeding. Expectant management was resumed and the tracing returned to category I. The patient subsequently began having recurrent late decelerations and was noted to be hypotensive with a blood pressure of 78/45 mm Hg. The FHR tracing is shown in Fig 5.Findings in Fig 5 were as follows: Intravenous fluids were administered. Anesthesia evaluation revealed an adequate epidural level. The epidural infusion was decreased and patient-driven epidural boluses were stopped. The maternal blood pressures subsequently improved to 105/65 mm Hg. A subsequent cervical examination showed 8-cm dilation, 90% effacement, and 0 station without evidence of cord prolapse. She had no vaginal bleeding.The patient progressed to become fully dilated and had an uncomplicated 19-minute second stage of labor resulting in a spontaneous vaginal delivery of a male infant weighing 3,516 g (63rd percentile) with Apgar scores of 9 and 9 at 1 and 5 minutes, respectively. Cord gases demonstrated an arterial pH of 7.23 with a base excess of −3. The infant had an uncomplicated hospital course and was discharged from the hospital on day 2 after birth.Labor pain experienced in the first stage of labor is typically diffuse and poorly localized. As the fetus descends in the late first or second stage the pain is predominantly somatic, and thus, better localized. Neuraxial approaches to labor analgesia provide pain relief with minimal maternal and neonatal adverse effects. More than 60% of women in the United States with a singleton pregnancy select neuraxial analgesia for intrapartum pain control. Neuraxial options include epidural, spinal, and CSE techniques. Maternal hypotension may result in a transient uterine hypoperfusion and subsequent fetal decelerations. The incidence of maternal hypotension from sympathetic blockade during the administration of neuraxial analgesia depends on the speed of onset of the block. Epidural, unlike spinal anesthesia, allows for slow titration of the anesthetic and is less likely to cause hypotension. (1)CSE is associated with a possible increased incidence of FHR changes compared with epidural alone. (2) Fetal bradycardia in these cases is attributed to the more rapid administration of intrathecal opioids independent of epidural-provoked maternal hypotension. One proposed explanation is that the onset of pain relief quickly lowers circulating levels of epinephrine and β-endorphins, leaving oxytocin and norepinephrine unopposed and thus leading to uterine tachysystole. (3) Uterine tachysystole is defined as more than 5 contractions in a 10-minute period; the definition may also refer to a prolonged uterine contraction resulting in decreased uteroplacental perfusion that manifests as a fetal deceleration. Nonetheless, there have been no clinically significant reported effects of neuraxial analgesia on rates of instrumental or cesarean delivery. (1)In a randomized trial of laboring patients assigned to CSE or epidural analgesia for pain relief, increased uterine tone (as documented using an intrauterine pressure catheter) with associated FHR abnormalities was noted at a significantly greater rate in the CSE group than in the epidural group. (4) For the occurrence of FHR abnormalities, elevation of uterine tone was the independent predictor. In this study, all episodes of fetal deceleration resolved after the uterine tachysystole was treated with hydration and suspension of oxytocin.A category II or III tracing may be the result of a transient or more chronic cause of uteroplacental insufficiency. Transient causes of uteroplacental insufficiency include maternal hypotension and uterine tachysystole. In category II tracings with decelerations, intrauterine resuscitation strategies may be used to optimize uteroplacental perfusion including maternal lateral positioning, intravenous fluid bolus, blood pressure support, and evaluation and treatment of tachysystole with a tocolytic as indicated. (5)In the current case, fetal decelerations occurred initially following an episode of uterine tachysystole; she was given a tocolytic and as the uterine tone decreased, the FHR improved. Additional fetal decelerations occurred in the setting of hypotension after CSE placement; with appropriate maternal blood pressure stabilization, the FHR recovered, indicating the importance of uterine resuscitative procedures. These intrauterine resuscitative maneuvers of treating uterine tachysystole with a tocolytic, changing the maternal positioning off the inferior vena cava, an intravenous fluid bolus to improve maternal blood pressure, and reducing or stopping oxytocin administration permitted FHR stabilization. Subsequently, labor could continue, resulting in a vaginal delivery with a reassuring neonatal outcome.
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