Amniotic Fluid Embolism

(Initial draft 3-1-13)

Definition: Amniotic fluid and fetal debris entering the systemic maternal circulation, with an
anaphylactic reaction causing sudden cardiovascular collapse, altered mental status, and DIC.

Pathogenesis: A breech in the physical barriers between maternal and fetal environment,
mainly at the level of the endocervical veins, uterine trauma sites, and the placental
attachment site. A pressure gradient that favors the entry of amniotic fluid from the uterus
into the maternal circulation must be present.

Incidence: Approximately 1 in 15,000 deliveries. Accounts for 14% of maternal deaths. The
second leading cause of maternal deaths. Maternal mortality rate has declined from an initial
rate of about 80% to a current level of 22% with improved recognition and immediate
treatment.

Risk factors:
Maternal age >35 Cesarean delivery Operative vaginal delivery
Placenta previa Preeclampsia/Eclampsia Polyhydramnios
Cervical laceration Uterine rupture Induction of labor

Not risk factors:

Elderly primigravidity Grand multiparity Previous cesarean section
Multiple gestation Fetal macrosomia Amniotic infection
PROM
Protective factors: Maternal age <20 Dystocia

Hemodynamic changes: Pulmonary vasoconstriction and increased pulmonary vascular

resistance (pulmonary hypertension) leading to cardiovascular collapse (right ventricular
failure followed by left ventricular failure). Hypoxemia results from severe ventilation-
perfusion mismatching due to intense vasoconstriction of the pulmonary vasculature that
occurs with the initial embolic event.

Coagulopathy: The presence of tissue factor in amniotic fluid potentially activates the
extrinsic pathway by binding with factor VII and this triggers clotting by activating factor X,
with the subsequent development of a consumptive coagulopathy. The activation of the
clotting cascade in the pulmonary vasculature may cause generation of microvascular
thrombosis, which could then cause vasoconstriction. DIC results from a consumption
coagulopathy.

Clinical manifestations:
Occurrence: AFE typically occurs during labor and delivery or in the immediate postpartum
period, although it can occur as late as 48 hours postpartum. 70% of cases occur before
delivery.

Presentation: Sudden cardiovascular collapse, with profound systemic hypotension cardiac

dysrhythmia, cyanosis, dyspnea or respiratory arrest, pulmonary edema or ARDS, altered
mental status, and hemorrhage associated with DIC. These cardinal signs and symptoms of
AFE can occur separately or in combination and in different degrees.
Hypotension, respiratory distress, and cyanosis: Up to 100% of cases
DIC: 50% of cases
Seizures: 20% of cases
Cause of death: Maternal death due to AFE is typically caused by sudden cardiac arrest,
hemorrhage from DIC, or the development of ARDS and/or multisystem organ failure after
initial survival of the acute event.

**Symptioms: (Immediate to over 4 hours later)

Breathlessness Chest pain Feeling cold
Lightheadedness Distress Panic
A feeling of pins & needles in the fingers Nausea and vomiting

These symptoms may indicate hypoxia and might give the first clue to the diagnosis of AFE
before collapse and hemorrhage occur.

Diagnosis: There is at present no test that can reliably confirm AFE in suspected cases.

AFE should be suspected in a woman experiencing 1 or more of the following findings during
pregnancy, labor and delivery, or up to 48 hours postpartum:

Hypotension and/or cardiac arrest

DIC
Coma
Seizures

Tests:
Laboratory: CBC, coagulation profile, arterial blood gases, cardiac enzymes, electrolytes. Type
and cross match for blood products.
EKG: Look for tachycardia with right ventricular strain, ST and T wave abnormalities, cardiac
arrhythmias or asystole.
Pulse oxymetry: Look for sudden drop in oxygen saturation.
Chest X-ray: Look for diffuse bilateral heterogeneous and homogeneous areas of increased
opacity (indistinguishable from acute pulmonary edema from other causes).
Transesophageal echocardiography: Look for severe pulmonary hypertension, acute right
ventricular failure with a leftward deviation of the interatrial and interventruicular septum,
and a cavity-obliterated left ventricle during the early phase of AFE.

Differential diagnosis:
Pulmonary thromboembolism Air embolism
Drug-induced allergic anaphylaxis Myocardial infarction
Cardiac arrhythmia Anesthetic complications (total spinal/epidural)
Peripartum cardiomyopathy Aortic dissection
Aspiration of gastric contents Reaction to local anesthetic drugs
Blood transfusion reaction Sepsis
Postpartum hemorrhage Uterine rupture
Placental abruption Eclampsia

Prognosis:
The national registry showed that among survivors, persisting neurological impairment was
reported in 61% of women and 50% of infants.

Recurrence:
No instances of recurrent AFE have been reported in the literature.
Treatment:

Transfer immediately to the ICU.

Management goal: Maintenance of oxygenation, cardiac output and blood pressure, and
correction of the coagulopathy.

Cardiac arrest: Cardiopulmonary resuscitation should be initiated immediately. If the

:(uterine evacuation after unsuccessful resuscitation may be therapeutic for the mother,
because the weight of the gravid uterus on the inferior vena cava impedes blood return to the
heart and decreases systemic blood pressure).

Initial management:
Rapid correction of maternal hemodynamic instability, which includes correction of hypoxia
and hypotension to prevent additional hypoxia and subsequent end-organ failure.

Oxygen should be administered immediately by whatever means necessary, including face

mask, bag-valve mask, or endotracheal intubation, in concentrations adequate to keep oxygen
saturation at 90% or higher.

Treatment of hypotension: Optimization of preload, with rapid volume infusion of isotonic

crystalloid solutions. Fluid therapy should be based on pulmonary artery catheter or
transesophageal echocardiography monitoring.

Treatment of refractory hypotension: Inotropes, such as dobutamine, dopamine and

milrinone, can be added, because B-adrenergic effects improve myocardial contractility in
addition to the a-adrenergic vasoconstrictor effects. Maintain systolic blood pressure at or
higher than 90 mmHg and arterial PaO2 of at least 60 mmHg, with acceptable organ perfusion,
as indicated by a urinary output of at least 0.5 mL/kg/h or greater than 25 mL/h.

Administration of blood components: First line treatment for correcting the coagulopathy and
potential severe hemorrhage associated with AFE.
Packed red blood cells: To maintain oxygen delivery to the tissues
Fresh frozen plasma
Platelets
Cryoprecipitate: Particularly useful to replenish clotting factors in lieu of FFP in
volume-restricted patients. Contains fibronectin which could
facilitate the removal of cellular and particulate matter from the
blood.
Recombinant activated factor VIIa: For severe DIC, resistant to conventional blood
product replacement.

Management of postpartum hemorrhage: Look for the usual causes of PPH such as atony
retained POC, or cervical or uterine lacerations. If bleeding is profuse and pharmacological
intervention is unsuccessful, a hysterectomy may be necessary.

Other less common therapeutic approaches:

Aprotinin and serine proteinase inhibitor FOY for DIC
Uterine artery embolization for severe PPH
Cardiopulmonary bypass
Pulmonary artery thromboembolectomy
(continued)
Thrombolysis with tissue-plasminogen activator
Continuous hemodiafiltration
Arteriovenous hemofiltration
Exchange transfusion
ECMO
Intraaortic balloon counterpulsation
Inhaled nitric oxide
Prostacyclin
Sildenafil

Use of heparin to treat consumptive coagulopathy and corticosteroids to induce

immunosuppression is very controversial and therefore should not be given.