Cardiovascular Collapse in Pregnancy: Implications of Amniotic Fluid Embolism on Maternal and Neonatal Outcomes

A 35-year-old woman (gravida 3, para 2002) with a history of asthma presents with decreased fetal movement at 40 3/7 weeks’ gestation. She had an otherwise uncomplicated pregnancy. The patient is admitted to the labor and delivery unit for an induction of labor given the concern of decreased fetal movement. Fetal testing results are reassuring.The patient begins receiving oxytocin. Approximately 2 hours later, there is spontaneous rupture of membranes, and 2 minutes after, she becomes acutely hypoxic and unresponsive. A Code Blue is called, although at that time, the patient has a faintly palpable pulse. Concurrently, there is fetal bradycardia (Figure 1), and an emergent cesarean delivery is called 6 minutes after she became unresponsive. Upon arrival to the operating room, the patient is found to be pulseless, and cardiopulmonary resuscitation (CPR) is immediately initiated. She is intubated by the anesthesia team. As there was no return of spontaneous circulation, a resuscitative cesarean delivery is performed within 4 minutes of arrival.Return of maternal spontaneous circulation is achieved after 6 minutes. The patient remains intubated with pressor support intraoperatively. A postpartum hemorrhage consistent with disseminated intravascular coagulation ensues; a massive transfusion protocol is initiated with numerous transfusions of blood components. Oxytocin injection, methylergonovine, and tranexamic acid are given. An intrauterine vacuum-induced hemorrhage control system (Jada; Organon Pro) is activated without improvement in bleeding. Therefore, an emergent supracervical cesarean hysterectomy is performed for surgical management of the hemorrhage. The maternal-fetal medicine, gynecologic oncology, and trauma surgery teams are consulted intraoperatively for assistance. The patient has a total estimated blood loss of 5 L and is transferred to the intensive care unit (ICU).The female neonate weighs 2990 g (14th percentile) at 40 3/7 weeks’ gestation and has an Apgar score of 3 and 8 at 1 and 5 minutes, respectively, with a cord pH of 7.22. She has respiratory distress requiring a short course of continuous positive airway pressure. She has a sepsis evaluation with negative results and an evaluation for neonatal encephalopathy with normal findings. She is discharged 3 days after birth without any concerns.In the ICU, the patient is found to have a dilated right ventricle on transthoracic echocardiography and receives dobutamine for pressor support. A presumptive clinical diagnosis of amniotic fluid embolism (AFE) is made. Extracorporeal membrane oxygenation is considered; fortunately, the patient spontaneously improves without this intervention. On postpartum day 2, she is extubated and weaned off supplemental oxygen and blood pressure support with progressive improvement, and she is transferred to floor-level care. She is ultimately discharged home in good condition on postpartum day 10 with close follow-up.The cause of this patient’s sudden onset cardiovascular collapse was clinically consistent with an AFE. The incidence of AFE is estimated to be 1 in 40 000 births; the condition is unpredictable and life-threatening to both members of the maternal-fetal dyad and frequently requires CPR, emergent delivery, and control of postpartum hemorrhage.1 A clear unifying cause of AFE is unknown; however, it is thought to be caused by entry of amniotic fluid or other fetal debris into the circulation of the pregnant individual, usually through a disruption in the maternal-fetal interface such as rupture of membranes. When the circulation of the pregnant person is exposed to fetal debris or amniotic fluid, proinflammatory cytokines, tissue factor, and endothelin can trigger an immunologic reaction causing endothelial dysfunction, pulmonary vasoconstriction, edema, and activation of the coagulation cascade.2 Associations of this condition include advanced maternal age, multiparity, multiple gestation, prior cesarean delivery, early gestational age, preeclampsia and eclampsia, polyhydramnios, intrauterine fetal demise, and placenta previa.An AFE classically presents as a sudden onset triad of hypoxia, hypotension, and coagulopathy.3 More specifically, the initial presentation may start as an abrupt change in mental status, which can progress rapidly toward a catastrophic event in the pregnant individual, such as loss of consciousness, respiratory collapse, or cardiac arrest. Disseminated intravascular coagulation occurs in most cases, which may manifest as bleeding at intravenous or surgical sites, a massive postpartum hemorrhage, and hypovolemic shock. Fetal status in the setting of an AFE mirrors the decompensation of the pregnant person.3The differential for sudden cardiopulmonary collapse in a pregnant patient should remain broad, as AFE is a diagnosis of exclusion. Potential cardiac causes include myocardial infarction, arrhythmia, and pulmonary embolism. There should also be consideration of seizures, eclampsia, sepsis, or an iatrogenic cause such as medication effects, anaphylaxis, or complications after anesthesia.3According to the 2015 American Heart Association guidelines,4 if cardiac arrest occurs in a pregnant patient and a fundal height is at or above the umbilicus, high-quality CPR must be immediately initiated. High-quality CPR requires the patient to be supine on a backboard with the team performing at least 100 uninterrupted compressions per minute with a depth of 5 cm, allowing full chest recoil between compressions, including 2 manual breaths every 30 compressions. In pregnancy, because supine positioning can cause aortocaval compression, it is critical to perform manual left uterine displacement of the uterus concurrently, which is preferable to the left lateral decubitus position.4 The Advanced Cardiac Life Support Algorithm should then proceed as in nonpregnant individuals, including oxygen supplementation, intubation, defibrillation, and anti-arrhythmic and vasopressor medications when indicated. Concurrent external fetal monitoring should not interfere with the algorithm. Given this short timeline, delivery should be completed at the location of the cardiac collapse rather than after transferring the patient to the operating room, unless the patient can be transferred within 2 minutes.5 After the resuscitative cesarean delivery, hemodynamic status can dramatically improve after relieving the aortocaval compression from the gravid uterus. Combs et al developed a simplified checklist outlining critical steps in AFE management to help reduce the team’s cognitive load during this challenging clinical scenario (Figure 2).5After resuscitation, management of hemodynamic instability and coagulopathy is paramount with a multidisciplinary care team that may involve maternal-fetal medicine specialists, anesthesiologists, critical care intensivists, and cardiologists. Mean arterial pressure should be maintained over 65 mm Hg, and active transfusion of blood products is likely necessary because disseminated intravascular coagulation is likely already present or imminent. Uterine atony should also be expected and treated with sequential use of uterotonics, mechanical methods such as an intrauterine vacuum device or tamponade balloon, or compression sutures. If atony and hemorrhage are refractory to these methods, hysterectomy should be performed.3An AFE causes right heart strain or right heart failure due to fetal debris causing the inflammatory obstruction in the pulmonary vasculature of the pregnant patient. Echocardiography can aid with this diagnosis, and use of vasopressors, endotracheal intubation, and avoidance of volume overload can assist with treatment.6Neonatal morbidity is significant in the setting of an AFE. Prior studies have demonstrated high mortality rates, around 21% to 22%, although these rates may be improving.7 One large population-based study examining neonatal outcomes after AFE found the current neonatal mortality rate to only be around 2.2%.7 In this 2009 study, the neonatal ICU (NICU) admission rate was 20%, and 11% of infants required intubation.7Rapid deterioration in the fetal heart tracing may be seen in the setting of an AFE, mostly in response to cardiovascular collapse in the pregnant person and lack of perfusion to the placenta. There are some cases in which a fetal bradycardia precedes rapid deterioration of the pregnant patient,8,9 thus highlighting the importance of prompt initiation of CPR to support perfusion of the pregnant individual and subsequent placental perfusion in these scenarios.10Early communication with the NICU team is critical if an AFE is suspected in a pregnant person, especially as a Code Blue call may not directly alert the neonatal providers. When resuscitative cesarean deliveries occur, sometimes in unexpected settings, it is also paramount to make sure equipment for neonatal intervention, including intubation and other resuscitative measures, is available.In summary, this case demonstrates the importance of early recognition of an AFE, rapid initiation of high-quality CPR and resuscitative cesarean delivery and hysterectomy, and successful neonatal supportive care in an acute setting. At this facility, annual mandatory multidisciplinary simulation includes scenarios with a resuscitative cesarean delivery and reviews on calling a Code Blue in the facility. Additionally, simplified checklists have been created that outline critical steps in AFE management to help decrease the cognitive load of this difficult clinical scenario (Figure 2). Fortunately, both maternal and neonatal outcomes were favorable.American Board of Pediatrics Neonatal-Perinatal Content SpecificationUnderstand the assessment of fetal well-being.Recognize maternal medical disorders and medications affecting the fetus and newborn infant.Understand pregnancy physiology.