2.1.

Definition of Amniotic Fluid Embolism

Amniotic fluid embolism (also referred to as anaphylactoid syndrome of pregnancy)
is most commonly referred to it in its abbreviated form, AFE. Originally defined as a
disease in 1941, it remains an unpreventable, unpredictable and often-fatal
complication of pregnancy.
AFE is characterized by acute and rapid collapse of mother and/or baby as a result of
an allergic-like reaction to amniotic fluid entering the maternal circulatory system. It
is important to note that many laboring mothers have amniotic fluid or fetal debris
enter into their circulatory system and do not suffer such a response. Most recently
(2018) a team of researchers led by Dr. Steven Clark found AFE is not the result of
pulmonary obstruction. It is most generally defined as a two-phase response:
The first phase is characterized by rapid respiratory failure and cardiac arrest. The
second phase is known as the hemorrhagic phase. The mother begins to bleed
profusely at the wound site; typically at the site of placental attachment or cesarean
incision. Disseminated intravascular coagulopathy (DIC) or consumptive
coagulopathy develops, which prevents coagulation.
AFE remains a diagnosis of exclusion; meaning all other possible clinical
explanations for the symptoms have been ruled out. It was once believed to be
diagnosed only through autopsy based on the presence of fetal material found in the
vasculature of the lungs. This is no longer a valid diagnostic criteria.
2.2.Etiology of Amniotic Fluid Embolism
Experts believe one or more of the following has to happen for AFE to occur:
 Ruptured membranes
 Ruptured uterine or cervical veins
 A pressure gradient from uterus to maternal veins
 Abdominal trauma during pregnancy

The exact mechanism of what causes AFE is unknown and it remains unpreventable.
The most recent research suggests a possible theory that it is an immune-related
response to pregnancy associated antigens, although nothing has been done to test this
exact theory. Further research is needed to investigate the causes of AFE so that it can
be determined if AFE is in any way predictable or preventable.

2.3.Pathophysiology of Amniotic Fluid Embolism

The pathophysiology of AFE is speculative. The initial respiratory reaction possibly
begins with transient pulmonary vasospasm. Although this possible transient
vasospasm has not been documented (probably because the signs and symptoms
appear so abruptly in a seemingly healthy person who is not being monitored via
invasive methods), vasospasm may be caused by amniotic microemboli that trigger
the release of arachnoid acid metabolites, and lead to pulmonary hypertension,
intrapulmonary shunting, bronchoconstriction and severe hypoxia. Exactly which
components of amniotic fluid actually cause this effect is unknown, but Clark
suggests that abnormal components such as meconium may play a role. Many experts
speculate that maternal mediators also may hove an influence: amniotic fluid activates
complement, leukotrienes, endothelin, syncytiotrophoblastic cells and megakaryocyte
in pulmonary vessels pulmonary mast cell tryptase. The second manifestation
includes negative inotropism and left ventricular failure resulting in increasing
pulmonary edema and hypotension quickly leading to shock. The third manifestation
is a neurological response to the respiratory and hemodinamic injury, which may
include seizures, confusion, or coma.