Amniotic Fluid Embolism

Introduction

• Amniotic fluid embolism is a potentially catastrophic obstetric complication.
• The true incidence of AFE is unknown because of significant variability in the diagnostic criteria and reporting methodology used.¹
• The mortality rate varies widely depending on the source, but may be as high as 60%.¹
• There is no definitive test used to diagnose AFE, and the signs and symptoms are nonspecific.

Etiology

• Emboli of fetal material alone are insufficient to trigger an AFE.
• The presence of fetal antigens leads to a cascade of inappropriately released inflammatory mediators (thromboxane, leukotrienes, prostaglandins, endothelins)^1-3 (Figure 1).

• The previously used term “anaphylactoid syndrome of pregnancy” may then be inaccurate as the cascade likely causes mast cell degranulation, as opposed to the other way around.²
• Risk factors for AFE are listed in Table 1.

Diagnosis

• AFE is a clinical diagnosis and there is no definitive test used to diagnose AFE.
• Commonly used clinical criteria have been established including:
  • Acute hypotension, cardiac arrest/collapse
  • Acute respiratory compromise
  • Coagulopathy
  • Onset during labor, cesarean delivery, dilation and evacuation or within 30 minutes postpartum
  • Absence of another clear cause or diagnosis
• Of note, AFE may also occur up to 48 hours postdelivery and after abdominal trauma, first trimester abortion, in the second trimester, and during an amnioinfusion.²
• The differential diagnosis is broad as many of the signs and symptoms are nonspecific (Table 2).

• Common signs and symptoms of AFE are listed in Table 3.

• There is a biphasic cardiovascular response during AFE.²

1. Within the first 30 minutes (Figure 2):

2. If the patient survives the first phase, left ventricular failure and pulmonary edema may result (Figure 3).

• With survival to the second phase, patients also concomitantly experience disseminated intravascular coagulation (DIC) and hemorrhage.
• However, AFE may present atypically with DIC and hemorrhage without preceding cardiovascular collapse.²

Management

• The treatment of AFE is largely supportive.¹
• Aggressive clinical management should focus on cardiovascular support, treatment of hypoxemia, and management of hemorrhage and coagulation abnormalities for the optimization of maternal and fetal well-being.
• Patients often present with cardiac arrest (Table 4).

• If there is evidence or high suspicion of acute RV failure, management includes:
  • Vasopressors (i.e., norepinephrine)
  • Inotropes (i.e., milrinone or dobutamine)
  • Pulmonary vasodilators (i.e., inhaled nitric oxide or epoprostenol)
  • Avoidance of excessive fluid administration
• If the patient remains hemodynamically unstable or requires prolonged CPR despite interventions, consider extracorporeal membrane oxygenation (ECMO).³

Disseminated Intravascular Coagulation

• Amniotic fluid contains tissue factor, which binds to factor VII and activates the coagulation cascade.³
• The coagulopathy is related to both consumption and hyperfibrinolysis.^2,3