Amniotic Fluid Embolism

The long-standing term amniotic fluid "embolism" implies a primarily mechanical, obstructive disorder, as occurs in thromboembolism or air embolism. However, because amniotic fluid is completely soluble in blood, it cannot cause obstruction. Furthermore, the minor amounts of fetal cells and tissue debris that may accompany the amniotic fluid into the maternal circulation are too small to mechanically obstruct enough of the pulmonary vascular tree to cause the marked hemodynamic changes that occur in this syndrome.

sepsis and septic shock.

The inflammatory response causes organ damage, particularly to the lungs and heart, and triggers the coagulation cascade, resulting in disseminated intravascular coagulation (DIC). The resulting maternal hypoxia and hypotension have profound adverse effects on the fetus.

Because maternal exposure to fetal antigens is likely fairly common during labor and delivery, it is not clear why only a few women develop amniotic fluid embolism. It is thought that different fetal antigens in varying amounts probably interact with unknown maternal susceptibility factors.

Amniotic fluid embolism usually manifests during and shortly after labor and delivery. The first sign may be sudden cardiac arrest. Other patients suddenly develop dyspnea and have tachycardia, tachypnea, and hypotension. Respiratory failure, with significant cyanosis, hypoxia and pulmonary crackles, often quickly follows. There is high risk of mortality.

Coagulopathy manifests as bleeding from the uterus and/or sites of incisions and venipuncture.

Uterine hypoperfusion causes uterine atony and fetal distress.

• Obstetric history and vital signs

• Coagulation blood tests

• Exclusion of other causes

Diagnosis of amniotic fluid embolism is suspected when the classic triad develops during labor or immediately after delivery:

• Sudden hypoxia

• Hypotension

• Coagulopathy

Diagnosis of amniotic fluid embolism is clinical and by excluding other causes of the following:

• Sudden cardiac arrest in young women (eg, myocardial infarction, coronary artery dissection, congenital heart disease)

• Acute respiratory failure (pulmonary embolism, pneumonia, high spinal block)

• Coagulopathy (eg, sepsis, postpartum hemorrhage, uterine atony)

Autopsy may detect fetal squamous cells and hair in the pulmonary circulation, but this finding does not confirm the diagnosis. Fetal cells are sometimes detected in patients who do not have clinical manifestations of amniotic fluid embolism.

• Critical care team and intensive care unit support

• Cardiopulmonary resuscitation

• Uterotonics

• Usually, red blood cell and cryoprecipitate transfusion

Amniotic fluid embolism is a life-threatening emergency and requires urgent management by a clinical team with obstetric and critical care experience and access to intensive care equipment. The Society for Maternal-Fetal Medicine has provided a concise checklist for the immediate management of amniotic fluid embolism to help obstetric practitioners respond rapidly and efficiently (1).

Respiratory arrest is managed with endotracheal intubation and maintenance of airway and oxygen flow. Heart rate is monitored and cardiopulmonary resuscitation is often required. To improve venous return from the vena cava, the patient is positioned in a lateral tilt or the uterus may be manually displaced. Fluid overload should be avoided, and vasopressors may be necessary. If maternal cardiac arrest does not resolve with other resuscitative interventions, operative delivery (referred to as a perimortem cesarean delivery or resuscitative hysterotomy) is recommended at 4 minutes with delivery of the fetus by 5 minutes. Delivery results in autotransfusion of the blood in the myometrial veins and the evacuated uterus no longer restricts venous return. Delivery can be critical for survival of a pregnant patient and a fetus that is a viable gestational age.