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Amniotic fluid embolism

Amniotic fluid embolism
Literature review current through: Jan 2024.
This topic last updated: Jan 05, 2023.

INTRODUCTION — Amniotic fluid embolism (AFE) is a rare and often catastrophic condition that appears to involve the initiation of a "cytokine storm" as a result of exposure to an unknown inciting antigen, possibly related to amniotic fluid contents, that typically occurs during labor or delivery [1-3]. Prompt recognition facilitates rapid initiation of potentially life-saving therapies.

AFE is reviewed here. An overview of the management of critically ill obstetric patients is available separately. (See "Critical illness during pregnancy and the peripartum period".)

DIAGNOSIS

Clinical diagnosis — AFE is a clinical diagnosis based upon the presence of the characteristic clinical findings and exclusion of other potential causes of these findings. The diagnosis should be suspected in pregnant or recently postpartum women who experience sudden cardiovascular collapse, severe respiratory difficulty and hypoxia, and/or seizures, particularly when followed by disseminated intravascular coagulopathy (DIC). However, all of these classic clinical findings are not present in all patients with AFE.

The condition generally arises during labor or soon after delivery, in the absence of other explanations for these findings. In many cases, the diagnosis is made retrospectively, after all investigative data, including autopsy data, have been collected.

Atypical cases, representing approximately one-fourth of all cases of AFE, may present with only acute respiratory failure and hypotension. Uncommonly, DIC may be the initial presenting feature or may be absent. (See 'Clinical findings' below.)

Contrary to popular belief, the identification of amniotic fluid debris (squamous cells, trophoblastic cells, mucin, and lanugo) in blood drawn from the distal end of a pulmonary artery catheter or on histopathology of lung tissue is not diagnostic of AFE since these findings can be found in the maternal circulation and lungs of women without AFE [4]. Furthermore, many women who have classic signs and symptoms of AFE and meet the diagnostic criteria described below do not show any histologic evidence of amniotic material on autopsy [5,6].

Diagnostic criteria — A working group of the Society for Maternal-Fetal Medicine (SMFM) and the Amniotic Fluid Embolism Foundation proposed a definition of AFE based on the presence of four diagnostic criteria, all of which must be present [7]. It provides standardization for research purposes but may be also useful clinically.

Criteria for AFE (all must be present):

Sudden onset of cardiorespiratory arrest OR hypotension (systolic blood pressure <90 mmHg) with evidence of respiratory compromise (eg, dyspnea, cyanosis, or peripheral oxygen saturation <90 percent).

Documentation of overt DIC using the scoring system of the Scientific and Standardization Committee on DIC of the International Society on Thrombosis and Haemostasis (ISTH) [8], modified for pregnancy:

Platelet count >100,000/mL = 0 points, <100,000 = 1 point, <50,000 = 2 points

Prolonged prothrombin time or international normalized ratio <25 percent increase = 0 points, 25 to 50 percent increase = 1 point, >50 percent increase = 2 points

Fibrinogen level >200 mg/dL = 0 points, <200 mg/dL = 1 point

A score ≥3 is compatible with overt DIC. Coagulopathy must be detected before hemorrhage itself can account for dilutional or shock-related consumptive coagulopathy.

Clinical onset during labor or within 30 minutes of placental delivery.

Absence of fever (≥38°C) during labor.

Most experts agree that the use of these criteria would clearly exclude any patients who do not have AFE but may not capture those with atypical AFE [9].

INCIDENCE — AFE is rare, ranging from 1.9 to 6.1 cases per 100,000 deliveries in a review of reports from Australia, Canada, the Netherlands, the United Kingdom, and the United States that used various criteria for diagnosis [10,11]. Epidemiologic data may overestimate the true incidence of AFE since many such studies include patients misdiagnosed as having AFE using nonspecific findings [12].

PATHOGENESIS — The pathogenesis of AFE is not clear. It is hypothesized that entry of amniotic fluid (which contains fetal cells and other antigenic material) into the maternal systemic circulation via a breach in maternal/fetal interface leads to abnormal activation of humoral and immunological processes and release of vasoactive and procoagulant substances, similar to the systemic inflammatory response syndrome [13,14]. Bacterial antigens may play a role instead of, or in addition to, fetal antigenic material.

As a result, pulmonary pressures usually become acutely elevated, the right ventricle (RV) pressure increases, and the RV begins to fail. Mechanical obstruction of pulmonary arteries from cellular components of and debris in amniotic fluid plays no role in this RV failure [15]. RV failure may subsequently lead to left ventricle (LV) failure and systemic hypotension. LV failure may also be a direct effect of hypoxic injury to the left ventricle, release of maternal inflammatory mediators, or a direct depressant effect of amniotic fluid on the myocardium [16].

Acute pulmonary hypertension also results in severe ventilation/perfusion mismatching, cardiogenic pulmonary edema, and hypoxemic respiratory failure [2,17]. Later, noncardiogenic pulmonary edema can occur in some patients. The likelihood of damage to the endothelial-alveolar membrane and a capillary leak syndrome is supported by observations of high protein concentrations in edema fluid and amniotic fluid debris in the sputum and alveolar spaces of these patients [16,18-20].

Activation of factor VII and platelets and release of inflammatory mediators likely activates the coagulation cascade, resulting in disseminated intravascular coagulopathy (DIC) and, in turn, ischemic distal organ dysfunction and multi-organ failure. Hemorrhage from DIC further contributes to hemodynamic instability. (See "Noncardiogenic pulmonary edema" and "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults".)

Cytokeratin staining of lung tissue at autopsy has shown pulmonary mast cells and stromal cells as well as occasional fetal cells around the pulmonary capillaries and inflammatory cells in the alveoli [18-20]. Although changes in several inflammatory markers have been described, including decreased complement levels (C3, C4, and C1 esterase inhibitor), elevated serum tryptase levels, and increased pulmonary mast cell activity, most studies of acute inflammatory markers have used normal pregnant women as controls, rather than critically ill women with conditions other than AFE, thus negating their diagnostic value for AFE [18,21-23].

RISK FACTORS — Many investigators have attempted to identify risk factors for AFE. Most aspects of the labor and delivery process have been evaluated using a “shotgun” approach to risk factor identification, and many have been linked with an increased risk for AFE, with some discordance among studies [3]. The identification of risk factors is hampered by the frequent inclusion of patients with conditions other than AFE in the large, population-based studies from which risk factors are derived.

Although no risk factors for AFE have been firmly established, cesarean delivery, instrumental vaginal delivery, placental abnormalities (previa, abruption, accreta), and preeclampsia/eclampsia have been cited as potential risk factors [3,11,24,25].

CLINICAL FINDINGS

Timing for onset of symptoms — In the majority of cases, AFE occurs during labor and delivery, or within 30 minutes postpartum. In one national registry, 70 percent of cases occurred during labor, 11 percent after vaginal delivery, and 19 percent during cesarean delivery [17].

AFE can also occur following a first or second trimester abortion (medical or surgical), miscarriage, amniocentesis, or abdominal/uterine trauma, but this is rare, and typically only described in case reports [17,24-30].

Signs and symptoms — In most patients (90 percent) the clinical presentation of AFE is abrupt, catastrophic, and rapidly progressive [31]. Classically, patients present with cardiorespiratory compromise or sudden hypoxia and hypotension, often accompanied or followed by noncardiogenic pulmonary edema and hemorrhage due to disseminated intravascular coagulopathy (DIC) [14]. In patients who develop AFE during cesarean delivery, the development of these manifestations may be delayed or blunted due to initial anesthetic interventions aimed to correct early vital sign changes initially presumed to be related to anesthesia. Clinical manifestations include:

Aura – Up to one-third of patients may experience a sense of sudden doom, chills, nausea and vomiting, agitation, anxiety, or change in mental status immediately preceding the event [17,31,32].

Sudden cardiorespiratory failure and/or arrest – AFE is a common etiology of intrapartum and postpartum cardiopulmonary arrest, but an unusual cause of antepartum cardiopulmonary arrest [33]. The vast majority of patients suddenly develop hypoxemic respiratory failure, hypotension from cardiogenic shock, and/or cardiovascular collapse/cardiac arrest. Typical clinical findings include oxygen desaturation, dyspnea, tachypnea, cyanosis, crackles, and occasionally, wheeze. Hypoventilation is unusual unless in the setting of respiratory arrest.

Cardiac arrest (ie, cessation of cardiac activity with hemodynamic collapse) is typically due to sustained pulseless ventricular tachycardia or ventricular fibrillation but may be caused by a bradyarrhythmia and/or asystole. (See "Pathophysiology and etiology of sudden cardiac arrest".)

If the patient survives the initial cardiorespiratory event, noncardiogenic pulmonary edema often develops (worsening dyspnea and tachypnea, crackles) as left ventricular failure resolves.

Hemorrhage – DIC causes hemorrhage in over 80 percent of patients with AFE [1,2,17,34]. It typically occurs shortly after the development of cardiorespiratory compromise but cases of AFE presenting with hemorrhage in the absence of antecedent cardiopulmonary compromise have been described [34,35]. In patients who have not delivered, prolonged bleeding from sites of invasive interventions such as intravascular lines are the most common manifestations of DIC. However, after vaginal and cesarean delivery, bleeding is more likely to originate from the uterus and incision/laceration sites. Spontaneous bleeding may also occur in the urinary and/or gastrointestinal tract.

Tonic-clonic seizures and/or stroke – These are rare initial manifestations and uncommon complications of AFE [17,36,37].

There may be less severe, atypical presentations of AFE in which only some of the major symptoms and signs occur [38-40]. The clinical course may be abbreviated and have a better prognosis, compared with women who have the full syndrome.

Laboratory and imaging

Coagulation – DIC is the key laboratory abnormality: Elevated D-dimer, low fibrinogen [especially <200 mg/dL], and thrombocytopenia occur in most patients [1,2,17], typically within 30 minutes after the onset of cardiopulmonary compromise. Uncommonly, laboratory abnormalities occur in the absence of cardiorespiratory compromise or are delayed (up to 48 hours after initial presentation) [2,41-43]. Rotational thromboelastometry has been reported anecdotally to help identify coagulopathy in patients with AFE who have no overt signs of bleeding [44]. (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Viscoelastic testing'.)

Complete blood count (CBC) – Additional laboratory findings are nonspecific and include anemia secondary to hemorrhage and, occasionally, an elevated white blood cell (WBC) count; however, a WBC up to 20,000 cells/microL can be a normal finding in laboring and postpartum women. (See "Maternal adaptations to pregnancy: Hematologic changes".)

Arterial blood gas (ABG) – ABG analysis typically reveals hypoxemia, which is often profound, and rarely hypercapnia. Metabolic acidosis occurs in those who have prolonged hypotension or cardiac arrest.

Chest radiograph – Chest imaging is often normal early in the course of the disease, but dense bilateral infiltrates consistent with pulmonary edema, acute respiratory distress syndrome, or hemorrhage may be seen as AFE evolves.

Electrocardiogram (ECG) – Electrocardiography typically reveals sinus tachycardia but may also reveal arrhythmias typical of those seen in cardiac arrest. (See "Overview of sudden cardiac arrest and sudden cardiac death".)

Echocardiography – Echocardiography reveals a rise in pulmonary pressures (usually lasting 15 to 30 minutes), followed by reduced left ventricular ejection fraction.

Fetal heart rate pattern — Maternal cardiorespiratory compromise and release of catecholamines before delivery leads to a decrease in uteroplacental perfusion, fetal hypoxemia, and then fetal acidosis, with characteristic changes in the fetal heart rate pattern (eg, absent baseline fetal heart rate [FHR] variability and late decelerations or terminal bradycardia). (See "Intrapartum category I, II, and III fetal heart rate tracings: Management".)

INITIAL EMERGENCY MANAGEMENT FOR UNSTABLE PATIENTS — A multidisciplinary, team-based approach involving maternal-fetal medicine, anesthesia, critical care, respiratory, and nursing is desirable to increase the chances of stabilization and avoid further deterioration, given that most patients present with acute cardiorespiratory compromise, hypoxemia, and hemorrhage from disseminated intravascular coagulation (DIC) [45]. The initial set of goals are to (table 1):

Perform cardiopulmonary resuscitation (CPR) – Most experts recommend "high quality CPR" (eg, rapid [100/minute] forceful [2 inch depth] chest compressions with time for adequate recoil and with minimal [no more than 5 to 10 seconds] interruption) [14]. When real CPR events are videotaped and reviewed, many times clinicians perform "low quality CPR."

Control hemorrhage and reverse coagulopathy – We recommend administering tranexamic acid (TXA) [46] and activating a massive transfusion protocol. (See "Massive blood transfusion".)

Confirm the presumptive diagnosis of AFE by excluding other diagnoses.

Deliver the fetus if the fetus is alive and beyond the gestational age of ex utero viability or if delivery will aid in maternal resuscitation. (See 'Delivery of the fetus' below.)

If this is achieved, further management is described below. (See 'Management of stable patients' below.)

Cardiopulmonary resuscitation

Basic and advanced cardiac life support — Initial strategies should focus on standard basic and advanced cardiac life support maneuvers to treat shock and cardiopulmonary compromise so that adequate tissue perfusion for both mother and fetus (if alive and not yet delivered) can be ensured. This typically involves manual chest percussions, emergency airway management with supplemental oxygen and intubation, and the establishment of intravenous (IV) access, if not already in place for fluid resuscitation and arrhythmia management. In general, time should not be wasted or resuscitation withheld while obtaining central IV access; in general, central venous access and monitoring catheters can be placed once the patient stabilizes.

Details of cardiac resuscitation that are specific to pregnancy (eg, uterine displacement to avoid aortocaval compression, intravenous access above the diaphragm, avoidance of alkalosis, lower than usual ventilation volumes, high fractions of inspired oxygen, fetal monitoring, and delivery) are discussed separately. (See "Sudden cardiac arrest and death in pregnancy".)

Hemodynamic support (fluids and vasopressors) — Initial resuscitation involves the rapid administration of IV fluids to restore tissue perfusion. In the absence of hemorrhage, crystalloids are generally used (eg, normal saline or lactated Ringer’s solution); there does not appear to be any robust mortality benefit to the administration of colloids in most cases of non-hemorrhagic shock (eg, albumin). However, in those with evidence of hemorrhage, blood is preferred but fluids should be administered until blood is available for transfusion. (See "Initial management of moderate to severe hemorrhage in the adult trauma patient" and "Treatment of severe hypovolemia or hypovolemic shock in adults", section on 'Choice of replacement fluid'.)

Fluids should be administered as rapid boluses (eg, 500 mL boluses) or infusions with frequent assessment of the response. The response should be acutely followed by the assessment of vital signs; novel tools for assessing the hemodynamic response to fluids have not been validated in pregnant women. Once the intravascular volume has been replenished or pulmonary edema becomes apparent, fluids should be discontinued. (See "Novel tools for hemodynamic monitoring in critically ill patients with shock", section on 'Vena cava assessment'.)

For patients who remain hypotensive after adequate resuscitation, initiation of vasopressor therapy, typically norepinephrine, is appropriate (table 2) [47]. The initial choice of vasopressor for pregnant patients with refractory hypotension is often individualized and determined by factors including the presence of coexistent conditions contributing to shock (eg, heart failure), arrhythmias, organ ischemia, or agent availability. In most cases norepinephrine is the agent of first choice. However, adding the inotrope, dobutamine, may be appropriate for those who have cardiogenic shock. Alternatives to norepinephrine are epinephrine (preferred in anaphylaxis), ephedrine (preferred for post anesthesia hypotension), or phenylephrine (preferred if tachyarrhythmia is an issue). Further details regarding vasopressor therapy in pregnant patients are discussed separately. (See "Critical illness during pregnancy and the peripartum period", section on 'Vasopressors' and "Use of vasopressors and inotropes" and "Evaluation and management of suspected sepsis and septic shock in adults", section on 'Vasopressors' and "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction", section on 'Vasopressors and inotropes'.)

Respiratory support — The management of respiratory failure is supportive and includes the administration of supplemental oxygen, and, in most cases, intubation and mechanical ventilation. Preferred settings are discussed separately. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit" and "Critical illness during pregnancy and the peripartum period", section on 'Mechanical ventilation' and 'Management of stable patients' below.)

Extracorporeal membrane oxygenation (ECMO) should not be used routinely. Since anticoagulation is required for ECMO, the risk of bleeding is increased in the patients with AFE, who commonly have DIC. However, several case reports suggest successful use in patients with refractory AFE, such as those unresponsive to standard ventilator maneuvers or undergoing prolonged cardiac arrest in whom oxygenation is required for fetal delivery [48-53]. Transfer to a facility with expertise in ECMO may limit the feasibility of the option. (See "Extracorporeal life support in adults in the intensive care unit: Overview".)

Management of hemorrhage and coagulopathy — Immediate, rapid transfusion of blood products is critical in patients who present with severe hemorrhage. Most obstetric units have a massive obstetric transfusion protocol in place, which should be followed. Fluids are transfused until blood arrives. Clinicians should monitor vital signs and overt bleeding: hemoglobin and hematocrit values are poor indicators of acute blood loss as they may not decline immediately after an acute bleed.

Even in absence of hemorrhage, treatment of coagulopathy is justified if the risk of bleeding is considered high (eg, surgery is anticipated). In patients who are bleeding or at high risk of bleeding, we typically administer the following for management of coagulopathy:

For patients with a platelet count <50,000/microL, we typically give one to two units of random donor platelets per 10 kg of body weight, or one single donor apheresis unit daily. The increase in platelet count may be less than expected due to ongoing platelet consumption.

For patients with a prolonged prothrombin time (PT) or activated partial thromboplastin time (aPTT), fresh frozen plasma (FFP) should be administered with the goal of reducing the international normalized ratio (INR).

For patients in whom the fibrinogen level is <200 mg/dL, cryoprecipitate and FFP should be administered. Each unit of cryoprecipitate usually raises the level of fibrinogen by 10 mg/dL (goal >100 mg/dL). FFP is administered to patients with an initial fibrinogen level <50 mg/dL because FFP is often immediately available and provided in the massive transfusion cooler while cryoprecipitate usually needs to be thawed and can take time to arrive at the patient's bedside. Some obstetric units have moved aggressively to use of lyophilized fibrinogen concentrate. (See "Disorders of fibrinogen", section on 'Fibrinogen concentrate: Dosing and monitoring'.)

There is no evidence to support prophylactic anticoagulation for DIC in the absence of thrombus. Further details regarding the management of DIC in pregnancy and complications of massive blood product transfusion are discussed separately. (See "Disseminated intravascular coagulation (DIC) during pregnancy: Clinical findings, etiology, and diagnosis" and "Evaluation and management of disseminated intravascular coagulation (DIC) in adults" and "Massive blood transfusion" and "Overview of postpartum hemorrhage".)

Recombinant human factor VIIa (rVIIa) has been used in patients with severe coagulopathy and bleeding, especially in those undergoing surgery to control postpartum hemorrhage [54,55]. However, some experts believe that its use is associated with thrombotic morbidity and mortality (eg, stroke and pulmonary embolism) [56]. We believe that factor VIIa use in patients with AFE should be reserved as a last resort and only for those with hemorrhage refractory to medical and/or surgical intervention. (See "Recombinant factor VIIa: Administration and adverse effects" and "Postpartum hemorrhage: Medical and minimally invasive management" and "Postpartum hemorrhage: Management approaches requiring laparotomy".)

Anecdotal evidence and case reports suggest that C1 esterase inhibitor concentrate [57], fibrinolytic agents such as aprotinin and aminocaproic acid, and a combination of atropine, ondansetron, and ketorolac (A-OK) have been successfully used [58]. However, their use remain investigational and, as such, reserved for refractory cases. These non-evidence based approaches should not be used instead of the standard approaches to treatment outlined in this section.

Delivery of the fetus — When AFE presents before delivery of a pregnancy >22 to 23 weeks of gestation, the need for immediate delivery must be determined. The decision is made on a case-by-case basis, but factors that generally mandate urgent delivery include a category III fetal heart rate tracing (ie, preterminal) in a fetus at or above the limit of viability (22 to 23 weeks of gestation), and/or rapid and progressive deterioration of the mother's condition since delivery of a fetus at or beyond this gestational age early in the resuscitation process theoretically may improve the chance of successful maternal resuscitation.

American Heart Association guidelines for cardiopulmonary arrest in pregnancy recommend beginning perimortem cesarean (resuscitative hysterotomy) at four minutes and completing delivery of the newborn by five minutes following cardiac arrest. In practice, such rapid delivery must be seen as an ideal goal, and is not always possible. (See "Sudden cardiac arrest and death in pregnancy", section on 'Delivery as part of the resuscitation process' and "Disseminated intravascular coagulation (DIC) during pregnancy: Clinical findings, etiology, and diagnosis".)

Major maternal morbidity or death is a significant risk when a cesarean delivery is performed in the presence of coagulopathy. If a cesarean delivery has to be performed urgently, blood, FFP, platelets, and cryoprecipitate should be available in the operating room and should be administered if there is any clinical evidence of impaired coagulation (eg, persistent bleeding without clotting from incision or needle sites).

Other — Anecdotal case reports describing use of intralipid as a component of successful resuscitation of patients with AFE have been published [59,60]. More data are needed before the efficacy of this approach can be determined.

ASSESSMENT AND TREATMENT OF POTENTIAL ETIOLOGIES

Initial testing — Since AFE is a diagnosis of exclusion, during resuscitation clinicians should simultaneously evaluate for and consider empirically treating competing etiologies that can cause cardiopulmonary compromise and hemorrhage in a pregnant patient. We perform the following tests:

Complete blood count with platelets

Serum electrolytes, blood urea nitrogen, creatinine, calcium, magnesium, phosphate

Liver function tests

Troponin-I

Brain natriuretic peptide

INR, activated partial thromboplastin time, fibrinogen

Blood type and antibody screening (if not done at admission)

Arterial blood gas

Bedside chest radiograph

Electrocardiography

Bedside ultrasonography (if available), including lower extremity, lung, and abdominopelvic ultrasonography, transthoracic echocardiography [61]; rarely, transesophageal echocardiography

Disorders that mimic the signs and symptoms of AFE — Several syndromes can mimic AFE. The most common postpartum obstetric conditions that have some common features with AFE are hemorrhage secondary to uterine atony, lower genital tract and uterine lacerations, retained placenta, and complications of neuraxial anesthesia. The key factor that distinguishes AFE from other disorders associated with life-threatening postpartum uterine bleeding is that coagulopathy AFE may be severe, and occurs before hemorrhage itself can account for dilutional or shock-related consumptive coagulopathy. Furthermore, in most patients, atony, lacerations, and retained placenta can be readily diagnosed on physical examination.

Before delivery, however, placental abruption can cause DIC out of proportion to the volume of vaginal blood loss. Nevertheless, a severe abruption can be distinguished from AFE by the presence of abdominal pain and uterine tetany and the absence of the sudden onset of cardiorespiratory arrest or hypotension in most patients. (See "Acute placental abruption: Pathophysiology, clinical features, diagnosis, and consequences", section on 'Clinical features of acute abruption' and "Overview of postpartum hemorrhage", section on 'Risk factors for PPH'.)

Medical disorders that can mimic AFE include pulmonary thromboembolism, anesthetic accident, myocardial infarction, and septic shock. In most patients, the distinguishing feature of AFE is the abrupt onset of the classic constellation of signs and symptoms together with the timing vis a vis labor and delivery (during labor or within 30 minutes of placental delivery). The use of the diagnostic criteria described above (eg, absence of fever) should help exclude all of these conditions. (See 'Diagnostic criteria' above.)

Conditions that mimic the signs and symptoms of AFE are discussed in detail below (table 3 and table 4).

Causes of cardiopulmonary compromise arrest — Although AFE is one of the common causes of cardiac arrest during labor [33], other common etiologies should be considered in patients who present with acute cardiorespiratory arrest/compromise and hypoxemia during labor and delivery, including:

Acute pulmonary embolism (PE; obstructive shock) – The absence of clinical coagulopathy in PE is helpful in distinguishing PE from AFE.

In unstable patients, emergency bedside lower extremity ultrasonography may reveal thrombus to support a diagnosis of PE and justify therapy. Alternatively, embolic material consistent with thrombus may be distinguished from air on bedside echocardiography, but identifying material in the inferior vena cava, right ventricle, or pulmonary artery is extremely rare in PE. Right ventricle enlargement on bedside echocardiography may be seen in both AFE and PE, and is therefore not useful. Similarly, D-dimer is unlikely to be helpful since many patients in the third trimester and patients with acute illness have elevated levels of D-Dimer. Once stable and the suspicion for PE remains, patients should undergo computed tomographic pulmonary angiography. Emergency management of unstable patients with PE is thrombolysis, provided there is no contraindication. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism" and "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults".)

Anaphylactic shock (distributive shock) – Anaphylactic shock may be distinguished from AFE by the presence of a provoking factor (eg, administration of antibiotics), clinical features supportive of anaphylaxis (lip and oropharyngeal swelling, inspiratory stridor, hives) and not observed in AFE, and absence of DIC.

The emergency management of suspected anaphylaxis includes intramuscular epinephrine, typically 0.3 mg of 1:1000 epinephrine injected into the mid-outer thigh and repeated every 5 to 15 minutes as needed (table 5). Following epinephrine, antihistamines (eg, diphenhydramine 25 to 50 mg and famotidine 20 mg intravenously), nebulized albuterol (2.5 mg in 3 mL of normal saline), and methyl prednisolone (1 to 2 mg/kg intravenously) are often administered. (See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock" and "Anaphylaxis during pregnancy and delivery".)

Septic shock (distributive shock) – Septic shock may be distinguished from AFE by presence of fever, suspected infectious source, leukocytosis with left shift, and coexistent hypovolemia. Overt DIC is common in AFE but infrequent in early sepsis, although coagulopathy is common. Many patients with septic shock have signs of hypovolemia; however, shock from hypovolemia is unlikely to present acutely during labor and delivery. Serum lactate is unlikely to be helpful since all states of shock may elevate lactate. Emergency management involves the early administration of fluids and targeted antibiotics, and for septic shock refractory to fluids, hydrocortisone (100mg intravenously every 6 to 8 hours). (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis".)

Cardiogenic shock – Cardiogenic shock from peripartum cardiomyopathy or myocardial infarction may be distinguished from AFE by the presence of crushing anterior chest pain, and in some cases, a known diagnosis of cardiomyopathy or risk factors for ischemic heart disease or arrhythmia (eg, known history of Wolf Parkinson White syndrome, prolonged QT syndromes). DIC is rare in early cardiogenic shock.

Bedside echocardiography may reveal a reduced left ventricular ejection fraction, which can be present in both cardiogenic shock and AFE but the presence of a regional wall motion abnormality, a pericardial effusion, or valve rupture would favor cardiogenic shock. Electrocardiography may show ST elevation classic of myocardial infarction or pericarditis and ST depression consistent with ischemia. Elevated brain natriuretic peptide levels occur during right or left ventricular ventricle stretch and as such may not be helpful in distinguishing cardiogenic shock from AFE. Emergency management involves inotropic support with vasopressors and, in some patients, intervention once stable. (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction".)

Anesthetic shock (distributive shock) – High spinal anesthesia and local anesthetic toxicity may occur in patients receiving anesthesia, but DIC is rare. Emergency management involves stopping the anesthetic and administering 20 percent lipid emulsion (bolus 100 mL IV over 2 to 3 minutes, followed by infusion of 200 to 250 mL over 15 to 20 minutes). (See "Local anesthetic systemic toxicity" and "Anesthesia for cesarean delivery" and "Adverse effects of neuraxial analgesia and anesthesia for obstetrics".)

Air embolism – Like AFE, air embolism presents suddenly, but DIC and hemorrhage are not typically present. Air embolism may be preceded by instrumentation (eg, cesarean delivery, central line placement) and can be diagnosed by visualization of air on bedside echocardiography (although air rapidly dissipates on imaging). Emergency management involves the administration of high fractions of inspired oxygen, and positioning on the left lateral side for venous embolism and supine for arterial embolism; transfer for hyperbaric oxygen should be considered, once the patient is stable. (See "Air embolism".)

Aortic dissection and tension pneumothorax are rare causes of cardiac arrest during labor and delivery.

The following A through H mnemonic was devised by the American Heart Association to help providers remember causes of cardiac arrest that should be considered in pregnant women [62]:

A: Anesthetic complications, Accident/trauma

B: Bleeding

C: Cardiac

D: Drugs

E: Embolic causes

F: Fever

G: General including hypoxia, electrolyte disturbances

H: Hypertension

Causes of DIC — Disseminated intravascular coagulopathy (DIC) has a wide differential (table 6) including sepsis, malignancy, trauma, transfusion reactions. The most common causes specific to obstetric patients include placental abruption and acute fatty liver of pregnancy, both of which can be readily diagnosed by history, physical examination, and laboratory studies. Although preeclampsia may cause thrombocytopenia, clinical DIC is not seen in this condition in the absence of placental abruption. (See "Disseminated intravascular coagulation (DIC) during pregnancy: Clinical findings, etiology, and diagnosis", section on 'Causes'.)

Maternal cardiovascular collapse and DIC from AFE can lead to uterine atony as a late finding [14]. In contrast, patients in whom the initial pathological event is uterine atony develop postpartum hemorrhage, which may then result in cardiovascular collapse and consumptive or dilutional coagulopathy if the hemorrhage is not controlled. It is a common diagnostic error to make the diagnosis of AFE based exclusively on hemorrhage with secondary coagulopathy caused by persistent atony [14]. (See "Overview of postpartum hemorrhage".)

Causes of acute respiratory failure — The differential diagnosis of acute respiratory failure in pregnancy is extensive and overlaps with many of the conditions discussed above that cause shock. In particular, acute respiratory distress syndrome (ARDS) and aspiration should be considered:

Most causes of ARDS are typically slower in onset and preceded by precipitating factors (eg, trauma, pneumonia). Chest imaging is typically abnormal and is necessary for the diagnosis of ARDS but may be normal in the early phase of AFE before pulmonary edema or non-cardiogenic edema develops. Mechanical ventilation strategies for ARDS are discussed separately. (See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults", section on 'Initial diagnostic evaluation' and "Acute respiratory distress syndrome: Ventilator management strategies for adults".)

Aspiration pneumonia may occur during labor and delivery and historically was a classic complication of cesarean delivery (Mendelson's syndrome). The aspiration may be witnessed but is otherwise indistinguishable from AFE. Chest imaging may be normal in the early phases of both aspiration and AFE. (See "Aspiration pneumonia in adults".)

Additional reasons for the development of acute respiratory failure occurring during pregnancy and the postpartum period are discussed separately. (See "Acute respiratory failure during pregnancy and the peripartum period", section on 'Disease-specific evaluation and management'.)

MANAGEMENT OF STABLE PATIENTS

Supportive care and monitoring — Once patients are delivered and stabilized, they should be transferred to the intensive care unit and, if indicated, undergo measures to eliminate competing etiologies.

For patients who are hemodynamically stable at presentation, management is supportive and focused on maintaining a secure airway and hemodynamic stability, the provision of adequate oxygenation, prevention of bleeding, and, if necessary, investigating remaining etiologies on the differential.

Airway and breathing – Ventilation should continue using principles that are in general similar to critically ill patients; although most AFE protocols classically state that lower than usual tidal volumes are preferred, most experts use tidal volumes of approximately 6 to 8 mL/kg ideal body weight (IBW), which is typical for non-acute respiratory distress syndrome (ARDS) patients. When/if ARDS develops, then low tidal volume ventilation is recommended (4 to 6 mL/kg IBW). There is no contraindication to the use of positive end-expiratory pressure (PEEP). The ideal fraction of inspired oxygen is unknown but we typically maintain peripheral oxygen saturation >96 percent. When respiratory failure or pulmonary hypertension is refractory, case reports describe successful use of extracorporeal membrane oxygenation (ECMO), inhaled nitric oxide or prostacyclin agonist, and ventricular assist devices as rescue measures [48,49,54,63]. Prone positioning is feasible with a gravid uterus but may be relatively contraindicated with a fresh cesarean delivery wound [64,65]. Further details on mechanical ventilation settings and rescue measures in patients with refractory respiratory failure are provided separately. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Settings' and "Acute respiratory distress syndrome: Ventilator management strategies for adults" and "Acute respiratory distress syndrome: Fluid management, pharmacotherapy, and supportive care in adults" and "Inhaled nitric oxide in adults: Biology and indications for use" and "Extracorporeal life support in adults in the intensive care unit: Overview" and "Short-term mechanical circulatory assist devices" and "Prone ventilation for adult patients with acute respiratory distress syndrome".)

Fluids and vasopressors – Once fluid resuscitation is considered adequate, fluids are generally weaned or discontinued. In cases where pulmonary edema develops, then diuresis may be needed. Clinicians should be aware that AFE is NOT a hypovolemic state and is commonly complicated by pulmonary edema or cardiogenic shock such that the excessive administration of fluids may worsen these complications. Thus, closely following resuscitation measures clinically or with hemodynamic monitors is advised. Similar to the acutely unstable patient, vasopressors are individualized but in general, patients with AFE, norepinephrine with or without dobutamine for any component of cardiogenic shock is reasonable. (See 'Hemodynamic support (fluids and vasopressors)' above.)

Treatment and/or prevention of bleeding – Hemodynamically stable patients with disseminated intravascular coagulopathy (DIC) and bleeding need replacement of blood and blood products and close follow up of their response until bleeding is controlled. (See 'Management of hemorrhage and coagulopathy' above.)

Hemodynamically stable patients with DIC but no evidence of bleeding requires a case by case approach. The decision to treat DIC in these patients is often dependent upon the estimated future risk of bleeding and should be made in conjunction with obstetric and hematology experts.

Further details regarding the management of DIC, complications of massive blood product transfusion, and vaginal bleeding are discussed separately. (See "Disseminated intravascular coagulation (DIC) during pregnancy: Clinical findings, etiology, and diagnosis" and "Evaluation and management of disseminated intravascular coagulation (DIC) in adults" and "Massive blood transfusion" and "Evaluation and differential diagnosis of vaginal bleeding before 20 weeks of gestation" and "Overview of postpartum hemorrhage".)

Other supportive care – In general, most patients require central venous and arterial access (typically not femoral unless postpartum) for frequent laboratory draws and hemodynamic monitoring. Pulmonary artery catheters are not typically placed unless there is an indication (eg, fluid status is unclear, pulmonary hypertension is suspected). Additional monitoring for volume status is intensive care unit (ICU)-dependent and discussed separately. (See "Pulmonary artery catheterization: Indications, contraindications, and complications in adults" and "Novel tools for hemodynamic monitoring in critically ill patients with shock".)

A course of corticosteroids should not be administered unless another indication for their use is present. (See "Glucocorticoid therapy in septic shock in adults" and "Acute respiratory distress syndrome: Fluid management, pharmacotherapy, and supportive care in adults", section on 'Glucocorticoids'.)

Routine ICU care should be administered including endotracheal tube care, gastrointestinal and venous thrombosis prophylaxis, nutrition support, glucose control, and ventilator associated pneumonia prevention measures. (See "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients" and "Acute respiratory distress syndrome: Fluid management, pharmacotherapy, and supportive care in adults" and "Glycemic control in critically ill adult and pediatric patients" and "Nutrition support in intubated critically ill adult patients: Initial evaluation and prescription" and "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults".)

Follow-up testing — Unstable patients should be followed with frequent laboratory draws (eg, every four to six hours) to monitor the response to therapy. This includes complete blood count with platelets, serum electrolytes, blood urea nitrogen, creatinine, calcium, magnesium, phosphate, liver function tests, prothrombin time, activated partial thromboplastin time, fibrinogen, D-Dimer, and arterial blood gas.

Depending upon clinical suspicion, further diagnostic imaging including transesophageal echocardiography and computed tomographic pulmonary angiography may be also needed to completely rule out competing etiologies such as aortic dissection, valvular heart disease, or pulmonary embolism. A follow-up chest radiograph is also prudent to evaluate for the development of cardiogenic pulmonary edema or ARDS which can complicate the later phases of AFE. Once all relevant data are obtained, the diagnosis of AFE may be confirmed. (See 'Diagnosis' above.)

PROGNOSIS — AFE is one of the leading causes of maternal mortality and is reported to cause 10 percent of all maternal deaths in developed countries [66]. Maternal mortality rates are high and prognosis in those who survive is poor.

The maternal mortality rate has been reported to range from 10 to 90 percent [1,11,17,67-72]. However, accurate rates are hampered by the lack of consensus on the definition of AFE [71]. While older reports generally suggest rates up to 90 percent, newer data report rates less than 50 percent, with an overall mortality of about 20 percent [67,71-74]. Many reports suggesting a lower mortality rate are based on administrative coding data and may contain a significant number of women with conditions other than AFE [3,7].

Complications/comorbidities substantially increase the risk of maternal mortality. In a cohort study of 14.6 million deliveries in the National Inpatient Sample from 2016 to 2019, the maternal mortality rate among patients who had AFE was 17 percent overall but 46 percent for patients with AFE, cardiac arrest, and coagulopathy; 43 percent for AFE, shock, and cardiac rhythm conversion; 39 percent for AFE, cardiac arrest, coagulopathy, and shock; 43 percent for AFE and placenta accreta spectrum; and 31 percent for AFE and placental abruption [11].

Hypoxemia, which is often profound, causes about 50 percent of the deaths that occur within the first hour [17,31]. Approximately 85 percent of patients with AFE die from cardiogenic shock or cardiac arrest [31].

Those who survive typically have a poor outcome, with as many as 85 percent suffering significant neurologic injury due to cerebral hypoxia [2,17], although patients with milder presentations likely have better outcomes. (See "Hypoxic-ischemic brain injury in adults: Evaluation and prognosis".)

If AFE occurs prior to delivery, neonatal outcomes are poor. The mortality rate is estimated to be between 20 and 60 percent and only up to 50 percent of survivors are neurologically intact [17,75]. Outcome is related to the time between maternal cardiopulmonary collapse and delivery, which ideally should be no more than four minutes [76].

Recurrence risk — While case reports suggest successful pregnancy following AFE, the risk of recurrence is unknown since no case of recurrent AFE has been reported [77].

Resources — Clinicians can submit cases and loved ones of patients with AFE can get support from foundations such as the AFE Foundation.

SUMMARY AND RECOMMENDATIONS

Epidemiology, pathogenesis and risk factors

Amniotic fluid embolism (AFE) is a catastrophic condition that typically occurs during labor or within 30 minutes postpartum.

AFE is rare (1 to 12 cases per 100,000 deliveries) and often lethal. (See 'Incidence' above.)

The pathophysiology of AFE is poorly understood but may be due to a vasospastic, inflammatory, and/or immune reaction to the presence of amniotic debris or other antigens in the maternal circulation. No useful identifying risk factors have been described. (See 'Pathogenesis' above and 'Risk factors' above.)

Clinical manifestations – AFE should be suspected in women who develop sudden cardiovascular collapse, hypoxemia, and hemorrhage in association with disseminated intravascular coagulopathy (DIC) during labor and delivery in the absence of other explanations. Uncommonly, DIC may be the initial presenting feature or may be absent. (See 'Clinical findings' above.)

Clinical sequelae, which rapidly ensue, include:

Cardiovascular: hypotension, arrhythmia, right and left heart failure, cardiogenic shock, cardiac arrest

Respiratory: hypoxemia, pulmonary edema, acute respiratory distress syndrome, respiratory arrest

Hematologic: hemorrhage coagulopathy, disseminated intravascular coagulation

Neurologic: seizure, altered mental status

Management of unstable patients – A multidisciplinary, team-based approach involving critical care, maternal-fetal medicine, respiratory care, nursing, and anesthesia specialists is preferred to increase the chances of stabilization and avoid further deterioration (table 1). In general, initial resuscitative efforts are simultaneous with diagnostic evaluation in an attempt to elucidate the etiology of cardiorespiratory compromise. An exact diagnosis is not required before starting life-saving supportive interventions. (See 'Initial emergency management for unstable patients' above.)

Initial strategies should focus on standard basic and advanced cardiac life support maneuvers to treat shock and cardiopulmonary compromise so that adequate tissue perfusion for both mother and fetus (if not yet delivered) can be ensured. This typically involves manual chest percussions, emergency airway management with supplemental oxygen and intubation, and the establishment of intravenous (IV) access, for fluid resuscitation and arrhythmia management. Vasopressors should be administered to those whose shock is refractory to resuscitative measures. (See 'Cardiopulmonary resuscitation' above and "Sudden cardiac arrest and death in pregnancy".)

For patients who present with hemorrhage, immediate and rapid transfusion of blood products is critical. In almost all suspected cases of AFE, activation of a massive transfusion protocol is recommended. (See 'Management of hemorrhage and coagulopathy' above and "Disseminated intravascular coagulation (DIC) during pregnancy: Clinical findings, etiology, and diagnosis" and "Massive blood transfusion".)

The need for immediate delivery must be determined on a case-by-case basis, but factors that favor urgent cesarean delivery include a nonreassuring fetal heart rate tracing of a fetus at or above the limit of viability and as part of the interventions for maternal resuscitation when the fetus is over 22 to 23 weeks of gestation. (See 'Delivery of the fetus' above and "Sudden cardiac arrest and death in pregnancy", section on 'Delivery as part of the resuscitation process'.)

During resuscitation clinicians should evaluate for and consider empirically treating competing etiologies that can mimic AFE (table 3 and table 4). This is achieved by a rapid initial examination of the skin, chest, abdomen and pelvis and preliminary investigations. Once stabilized, a more thorough investigation can be undertaken. (See 'Assessment and treatment of potential etiologies' above.)

Management of stable patients – For patients with suspected AFE who become stable after initial resuscitation or patients who are hemodynamically stable at presentation, management is supportive and focused on maintaining a secure airway and hemodynamic stability, the provision of adequate oxygenation, prevention of bleeding, and, if necessary, investigating remaining etiologies on the differential. (See 'Management of stable patients' above.)

Diagnosis – AFE is a clinical diagnosis that is based upon the constellation of classic clinical findings (abrupt cardiorespiratory compromise, hypoxemia, and hemorrhage in association with coagulopathy or DIC during labor or within 30 minutes postpartum) and the exclusion of other causes of the presenting symptoms. The identification of amniotic fluid debris (squamous cells, trophoblastic cells, mucin, and lanugo) in blood drawn from the distal end of a pulmonary artery catheter or in histologic lung tissue (biopsy or autopsy) is not helpful. (See 'Diagnosis' above.)

Prognosis – Maternal mortality due to AFE remains high, although less than in previous years, with an overall mortality of approximately 20 percent. However, even those who survive have significant morbidity including neurologic injury due to cerebral hypoxia. (See 'Prognosis' above.)

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References

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