Amniotic Fluid Embolism · What It Is, Causes, Signs and Symptoms, Treatment, and More

Published: Feb 19, 2026

Author: Emily Miao, MD, PharmD•

Editor: Alyssa Haag, MD•

Editor: Lily Guo, MD•

Editor: Kelsey LaFayette, DNP, ARNP, FNP-C

Illustrator: Abbey Richard, MSc

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What is amniotic fluid embolism?

Amniotic fluid embolism (AFE) is a life-threatening emergency that can occur during pregnancy, labor, or in the immediate postpartum period. It occurs when amniotic fluid (i.e., the fluid that bathes and surrounds the fetus during pregnancy) or fetal cells enter the circulation of the pregnant person. AFE is characterized by sudden cardiorespiratory arrest and may lead to life-threatening complications such as disseminated intravascular coagulation, which is a rare, life-threatening blood clotting disorder characterized by coagulation dysfunction, organ damage, and thrombosis.

AFE is associated with high mortality and morbidity and is the leading cause of peripartum cardiac arrest and the second leading cause of peripartum pregnant person deaths in the United States. It affects approximately 2 to 8 individuals per 100,000 deliveries.

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What causes amniotic fluid embolism?

AFE is an obstetric emergency that occurs when amniotic fluid and fetal cells enter the pregnant person’s circulation. The mechanism by which this occurs is poorly understood but is thought to result from the rupture of amniotic membranes or uterine veins either during pregnancy, labor, or delivery. Rarely, this can occur with trauma to the abdomen and high-risk procedures such as amniocentesis.

After the rupture of the amniotic membranes, fetal substances enter the pregnant person’s circulation, and the body’s immune response to amniotic fluid triggers a sequelae of life-threatening events. Since the fetal and pregnant person’s circulation are normally separated during pregnancy, the body’s immune system does not recognize fetal substances and considers them “foreign.” The immune system releases inflammatory cytokines (i.e., small proteins that regulate and communicate with immune cells) into the blood. It activates the complement (i.e., immune mediators which enhance antibody phagocytosis and immune clearance) and coagulation cascades. This leads to a combination of downstream effects including vasoconstriction in the respiratory vasculature, resulting in high pulmonary artery pressures. The elevated pressures in the respiratory system eventually cause cardiac dysfunction including strain on the right heart ventricle and heart failure. Meanwhile, activation of the coagulation cascade leads to disseminated intravascular coagulation and the formation of clots within the vasculature, which further contributes to hypoxia and multiorgan failure.

Risk factors for amniotic fluid embolism include advanced age of the pregnant person, multiparity (i.e., history of multiple pregnancies), cesarean section delivery, polyhydramnios (i.e., excessive amniotic fluid), placental abruption (i.e., condition where the placenta separates from the uterine wall before delivery), placenta previa (i.e., condition where the placenta partially or completely covers the cervix), and uterine rupture.

What are the signs and symptoms of amniotic fluid embolism?

Signs and symptoms of AFE include sudden, abrupt shortness of breath either during pregnancy, labor, or immediately following delivery. Signs of cardiorespiratory compromise such as extremely low blood pressure, tachycardia, and cyanosis, which is the blue discoloration of the skin and mucous membranes secondary to poor tissue perfusion, may be present. Signs of disseminated intravascular coagulation include bleeding from venipunctures or surgical sites, hematuria (i.e., blood in urine), bruising, and petechiae (i.e., pinpoint bleeding underneath the skin). Neurologic symptoms include altered mental status, confusion, and rarely, seizures if neurologic vasculature becomes compromised. If AFE is not detected and managed early, it can progress to cardiopulmonary arrest and death.

How is amniotic fluid embolism diagnosed?

Currently, there are no reliable, definitive tests that confirm the diagnosis of AFE. AFE is a diagnosis of exclusion that begins with a thorough review of symptoms and medical history. Laboratory blood tests including a complete blood count to evaluate platelet count, basic metabolic panel, liver function tests, serum fibrinogen, and coagulation studies (i.e., PT/PTT, INR) may help assess clotting function and organ dysfunction. Other supportive adjunctive tests include arterial blood gas, bedside chest radiograph, and electrocardiography.

The Society for Maternal-Fetal Medicine (SMFM) and the Amniotic Fluid Embolism Foundation have provided a case definition of amniotic fluid embolism and proposed diagnostic criteria to facilitate timely recognition and diagnosis. It also provides standardization of definitions for amniotic fluid embolism in research studies. They propose to diagnose AFE, all four of the following criteria must be met:

(1) Sudden cardiorespiratory arrest OR hypotension (i.e., systolic blood pressure <90 millimeters of Mercury [mmHg]) with evidence of respiratory compromise (e.g., cyanosis, peripheral oxygen saturation <90%)

(2) Documentation of disseminated intravascular coagulation with a score >3, using the standardized scoring system modified for pregnancy:
a) Platelet count >100,000/milliliter (ml) = 0 points; <100,000 = 1 point; <50,000 = 2 points
b) Prolonged PT or INR <25% increase = 0; 25 to 50% increase = 1 point; >50% increase = 2 points
c) Fibrinogen level >200 milligrams per deciliter (mg/dl) = 0 points; <200 mg/dl = 1 point

(3) Onset of signs and symptoms during labor or within 30 minutes of placental delivery
(4) Absence of fever (>38 C) during labor

How is amniotic fluid embolism treated?

Treatment of AFE consists of prompt delivery of the fetus and supportive care measures which include immediate resuscitation, hemodynamic support, and correction of the underlying etiology. Use of vaginal forceps or vacuum in a vaginal delivery, or emergent cesarean section can be considered to promptly deliver the fetus.

Immediate resuscitation and cardiac life support maneuvers include airway management (e.g., intubation), intravenous access establishment, and supplemental oxygen. Hemodynamic support strategies include the administration of intravenous fluids for hydration. If severe hypotension or shock occurs, vasopressors (e.g., norepinephrine) may be used to maintain organ perfusion.

Coagulopathy is managed using a 1:1:1 ratio of packed red blood cells, platelets, and fresh frozen plasma to replace the excess consumption of clotting factors seen in disseminated intravascular coagulation. In severe, refractory cases of cardiogenic shock, extracorporeal membrane oxygenation (ECMO), is a last-resort option. ECMO is a form of artificial life support that helps the heart and lungs function as the body recovers from severe illness.

What are the most important facts to know about amniotic fluid embolism?

Amniotic fluid embolism (AFE) is a life-threatening emergency that can occur during pregnancy, labor, or in the immediate postpartum period. AFE is an obstetric emergency that occurs when amniotic fluid and fetal cells enter the circulation of the pregnant person. Signs and symptoms of AFE include cardiorespiratory compromise, and sudden, abrupt shortness of breath either during pregnancy, labor or immediately following delivery. Amniotic fluid embolism diagnosis and management should be addressed simultaneously, as delays in care increase the risk of death. The clinical diagnosis of amniotic fluid embolism is made using proposed diagnostic criteria set forth by The Society for Maternal-Fetal Medicine (SMFM) and the Amniotic Fluid Embolism Foundation. These criteria also help streamline definitions used for amniotic fluid embolism research. Treatment of AFE consists of prompt delivery of the fetus and supportive care measures which include immediate resuscitation, hemodynamic support, and correction of the underlying etiology.

Key Takeaways

Definition	Amniotic fluid embolism (AFE) is a life-threatening emergency that can occur during pregnancy, labor, or in the immediate postpartum period in which amniotic fluid or fetal cells enter the circulation of the pregnant person potentially causing sudden cardiorespiratory arrest and life-threatening complications such as disseminated intravascular coagulation.
Epidemiology	- High mortality and morbidity - Leading cause of peripartum cardiac arrest - Second leading cause of peripartum pregnant person deaths in the U.S. - 2-8 individuals per 100,000 deliveries
Causes	Hypothesized mechanism: - Rupture of amniotic membranes or uterine veins (pregnancy, labor, delivery, or trauma to the abdomen and high-risk procedures) - Fetal substances enter pregnant person’s circulation → immune reaction (cytokine release → complement and coagulation cascade activation) → sequelae of life-threatening events - Vasoconstriction → high pulmonary artery pressures → cardiac dysfunction and heart failure - Activation of coagulation cascade → disseminated intravascular coagulation (DIC) → hypoxia, multiorgan failure Risk factors: - Advanced age of the pregnant person - Multiparity - Cesarean section delivery - Polyhydramnios - Placental abruption - Placenta previa - Uterine rupture
Signs and Symptoms	- Sudden shortness of breath during pregnancy, labor, or immediately following delivery - Signs of cardiorespiratory compromise - Low blood pressure, tachycardia, cyanosis - Signs of DIC: - Bleeding from venipunctures or surgical sites, hematuria, petechiae - Neurological symptoms: - Altered mental status, confusion, seizures - If not detected and managed → progression to cardiopulmonary arrest and death
Diagnosis	- Diagnosis of exclusion, no definitive tests - Laboratory test: complete blood count, basic metabolic panel, liver function tests, serum fibrinogen, coagulation studies - Other supportive tests: arterial blood gas, bedside chest radiograph, electrocardiography - Proposed diagnostic criteria (all four must be met): - Sudden cardiorespiratory arrest OR hypotension with evidence of respiratory compromise - Documentation of DIC with a score >3, using the standardized scoring system modified for pregnancy - Onset of signs and symptoms during labor or within 30 minutes of placental delivery - Absence of fever (>38°C) during labor
Treatment	- Prompt delivery of the fetus - Supportive care: - Immediate resuscitation - Hemodynamic support (IV fluids, vasopressors if shock) - Correction of underlying etiology - Packed RBCs, platelets, and fresh frozen plasma (DIC correction) - Severe, refractory cases: ECMO

References

Alhousseini A, Romero R, Benshalom-Tirosh N, et al. Nonovert disseminated intravascular coagulation (DIC) in pregnancy: a new scoring system for the identification of patients at risk for obstetrical hemorrhage requiring blood product transfusion. J Matern Fetal Neonatal Med. 2022;35(2):242-257. doi:10.1080/14767058.2020.1716330

Fong A, Chau CT, Pan D, Ogunyemi DA. Amniotic fluid embolism: antepartum, intrapartum and demographic factors. J Matern Fetal Neonatal Med. 2015;28(7):793-798. doi:10.3109/14767058.2014.932766

Pacheco LD, Clark SL, Klassen M, Hankins GDV. Amniotic fluid embolism: principles of early clinical management. Am J Obstet Gynecol. 2020;222(1):48-52. doi:10.1016/j.ajog.2019.07.036

Patient Safety and Quality Committee, Society for Maternal-Fetal Medicine. Electronic address: [email protected], Combs CA, Montgomery DM, Toner LE, Dildy GA. Society for Maternal-Fetal Medicine Special Statement: Checklist for initial management of amniotic fluid embolism. Am J Obstet Gynecol. 2021;224(4):B29-B32. doi:10.1016/j.ajog.2021.01.001

Stafford IA, Moaddab A, Dildy GA, et al. Amniotic fluid embolism syndrome: analysis of the Unites States International Registry. Am J Obstet Gynecol MFM. 2020;2(2):100083. doi:10.1016/j.ajogmf.2019.100083

Society for Maternal-Fetal Medicine (SMFM). Electronic address: [email protected], Pacheco LD, Saade G, Hankins GD, Clark SL. Amniotic fluid embolism: diagnosis and management. Am J Obstet Gynecol. 2016;215(2):B16-B24. doi:10.1016/j.ajog.2016.03.012