Open Journal of Obstetrics and Gynecology, 2011, 1, 178-183
doi:10.4236/ojog.2011.14034 Published Online December 2011 (http://www.SciRP.org/journal/ojog/
OJOG
).
Published Online December 2011 in SciRes. http://www.scirp.org/journal/OJOG
Amniotic fluid embolism: literature review and an integrated
concept of pathomechanism
Mieczysław Uszyński
Department of Propedeutics of Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University, Toruń, Poland.
Received 27 July 2011; revised 31 August 2011; accepted 22 September 2011.
ABSTRACT
Literature concerning procoagulant activity of the
amniotic fluid and pathomechanism of amniotic fluid
embolism (AFE) was surveyed and a new concept of
its pathogenesis, called the integrated concept of AFE,
was presented. According to this concept, two com-
ponents of the amniotic fluid are involved: 1) apop-
tosis-affected amniotic cells showing a special role in
the initiation of disseminated intravascular coagula-
tion (DIC) and 2) leukotrienes (formerly called slow-
reacting substances), inducing bronchial and pulmo-
nary vascular smooth muscle contraction. Although
each of these components initiates a different patho-
genic pathway, they both lead to the formation of a
mechanical barrier on blood flow through the lungs
(amniotic debris + microemboli) and/or functional
barrier (pulmonary vasoconstriction). An old dilem-
ma, concerning indications for heparin therapy in
AFE was recalled in the light of the new concept.
Keywords: Amniotic Fluid Embolism; Amniotic Cells;
Tissue Factor; Leukotriens; Disseminated Intravascular
Coagulation; Pulmonary Vasoconstriction
1. INTRODUCTION
Amniotic fluid embolism (AFE) is a rare but serious
condition that affects, according to earlier figures, 1 - 15
cases per 100,000 births, with a case fatality rate ranging
between 13% and 86%, whereas according to one of the
latest figures 7.7 per 100,000 births, with a case fatality
rate of 21.6% (for ref. see: [1]). It is most common dur-
ing labor (70%), although it may also develop after na-
tural delivery (11%) and during or after Cesarean section
(19%) [2].
AFE has been diagnosed since 1941, when two Ame-
rican gynecologists, Steiner and Lushbaugh [3], descri-
bed eight cases of sudden death of childbearing women
It was only after their publication that Meyer’s report of
1926 was noticed—the description also based on the pa-
thomorphology of the lung tissue [4].
Two clinical forms of AFE can be distinguished: 1)
typical, (classic) with three phases (phase 1—respiratory
and circulatory disorders, phase 2—coagulation distur-
bances of maternal hemostasis, phase 3-acute renal fai-
lure and acute respiratory distress syndrome (formerly:
adult respiratory distress syndrome, ARDS), and 2) aty-
pical, without the phase of respiratory-circulatory disor-
ders, beginning with hemostasis disorders in the mother
e.g. uterine hemorrhage or sometimes ARDS and renal
failure.
Three theories explain the pathomechanism of respi-
ratory-circulatory disorders and coagulation disturbances
in AFE, each of which have different premises. Briefly,
according to the mechanical theory, fetal squames and
other morphotic and amorphotic components of the fluid
act as a causative factor, blocking the pulmonary circu-
lation; the thromboplastin theory states that the obstruct-
tion is due to disseminated intravascular coagulation
(DIC), whereas according to the leukotriene theory, it is
leukotrienes that cause catastrophic pulmonary vasocon-
striction.
In the last 20 years, there have appeared case reports
of amniotic fluid embolism that cannot be explained by
any of the known theories. This mainly refers to the
cases of atypical embolism [5-8]. For instance, we can-
not explain the mechanism of isolated disseminated in-
travascular coagulation based on the leukotriene theory.
2. STUDY OBJECTIVE
The objectives of the study were to: 1) assess, based on
literature survey, thrombogenic potential of the amniotic
fluid; 2) discuss discrepancies between the existing theo-
ries of amniotic fluid embolism; 3) present a novel con-
cept of AFE which eliminates the discrepancies con-
cerning the pathomechanism of this complication and
takes into consideration new clinical and laboratory ob-
servations.

M. Uszyński / Open Journal of Obstetrics and Gynecology 1 (2011) 178-183 179
2.1. Historical Considerations Concerning the
Mechanism of AFE
a) Pioneer researchers of AFE, Steiner and Lushbaugh
[3], believed that cardiopulmonary collapse was caused
by disseminated pulmonary embolism of amniotic debris
of fetal origin (squamous cells, lanugo hairs, mucus th-
reads and fat droplets), and not by a biochemical mecha-
nism (mechanical theory of AFE).
b) Many authors—at first Weiner, Reid and Roby in
1949 [9], and later also others—based their explanations
on the presence of tissue factor (TF; formerly called tis-
sue thromboplastin), a procoagulant, in the amniotic
fluid. When the amniotic TF gets to the pulmonary arte-
rioles, it induces, as they thought, intravascular coagula-
tion. The microemboli block blood flow through the
lungs and what is more, consumption coagulopathy oc-
curs (in this way respiratory and circulatory disorders
were explained from the point of view of thromboplastin
theory).
c) The premises of the leukotriene concept of AFE
were first described in the years 1985 and 1986 [10,11],
though an overview of the theory contents was provided
in 1990 [12]. The animal studies revealed that infusion
of these substances resulted in severe pulmonary hyper-
tension followed by systemic hypotension with negative
inotropic effect and decreased cardiac output. It was
assumed that the action observed in animals could occur
in humans as well. According to this theory, metabolites
of the arachidonic acid cascade—mainly leukotrienes,
previously known as slow-reacting substance, but also
thromboxan A2 (TXA2) and others-cause catastrophic
pulmonary vasoconstriction in amniotic fluid embolism.
These metabolites either pass to the lungs with the am-
niotic fluid or are formed in loco after the fluid gets to
the pulmonary vessels.
The leukotriene concept of AFE has predominated
over the previous concepts. However, the search for po-
tent vasoconstrictors and bronchoconstrictors that could
induce embolic symptoms is still continued. Currently,
there are three or even four candidates: leukotrienes +
endothelin-1 + bradykinin + thrombin (see below). How-
ever, whether the action of these substances on the pul-
monary vessels and bronchi is synergistic still remains
unknown.
d) In 1995, hypoxia in AFE was suggested to stimu-
late local production (in the lungs) of endothelin-1 which
is a known potent vasoconstrictors and bronchoconstric-
tors (experimental studies) [13]. Later it was reported
that amniotic squames could also be the source of endo-
thelin-1 [14].
e) In 2005, the role of bradykinin in the pathogenesis
of respiratory and circulatory disorders in AFE was dis-
cussed [15]; bradykinin was suggested to cause contrac-
tion of smooth muscles of the lungs and bronchi, and to
impair pulmonary microcirculation. As far as kinins are
concerned, kininogenesis is a process associated with
coagulation and fibrinolysis. Two factors are a common
link, namely kallikrein and high-molecular kininogen
(HMK). Under the effect of kallikrein, three kinins are
formed from kininogen: Met-kallidin, kallidin and bra-
dykinin. Kinins are degraded by kininases. All compo-
nents of the kininopoietic system have been found in the
amniotic fluid [16]. The most active of the kinin group is
nanopeptide bradykinin.
f) In 2009, Zhou et al. [17] identified (described) the
presence of phosphatidylserine (PS) in amniotic cells
and showed its role in the process of thrombin produc-
tion. The involvement of amniotic cells in the generation
of thrombin is the key to the elucidation of DIC mecha-
nism in AFE (see further).
2.2. Formation and Composition of the
Amniotic Fluid (Remarks)
In the second half of the gestation period, amniotic fluid
is mainly a product of the fetus and only to a small ex-
tent generated by fetal membranes. Fetal excretions pass
directly to the fluid (primary urine, lung, oral and nasal
excretion). They contain epidermal cells, fetal lanugo
and sebaceous gland secretions from the fetal skin (ver-
nix caseosa), desquamated bronchial cells, nasopharyn-
geal cells and urinary tract cells as well as desquamated
cells of the umbilical cord and fetal membranes. In the
case of fetal distress (asphyxia, intrauterine infection),
meconium is excreted from the alimentary tract of the
fetus to the fluid [18,19].
2.3. Procoagulants and Anticoagulants
in Amniotic Fluid
In the past, as a rule, procoagulants, anticoagulants and
fibrinolytic components were searched only in the su-
pernatant, whereas sediment was treated as a biologi-
cally inactive material. The first report on the distribu-
tion of procoagulants in the two fluid fractions, i.e. su-
pernatant and sediment, appeared only in the last ten
years. It has been found that TF is a predominant pro-
coagulant in the supernatant, whereas other coagulation
factors show only a few percent of the global procoagu-
lant activity; TF and a few coagulation factors in an ac-
tive form (IIa, VIIa and Xa) were detected in sediment
[20].
The amniotic fluid does not contain fibrinogen ,factors
V and VIII, but it has all other procoagulants (coagula-
tion factors: II, TF, VII, IX, X-XIII, prekallikrein and
high molecular kininogen, HMK) and anticoagulants (ti-
ssue factor pathway inhibitor, TFPI; antithrombin, AT;
protein C and S; thrombomodulin, TM), which were i-
dentified by activity or antigen. The levels of procoagu-
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lants and anticoagulants are very low as compared to the
plasma (3% - 5% of plasma value). The exception is TF,
whose level in the fluid is higher than in the plasma (for
ref. see: [21]). The higher-molecular weight (46,000)
form of TF predominates in amniotic fluid (in tissues
40,000 - 46,000) [20]. It is assumed that the major sour-
ce of TF in amniotic fluid is the cells of desquamated e-
pidermis of the fetus.
There is evidence for the functioning of the coagula-
tion cascade in amniotic fluid, although its range is in-
complete due to a lack of fibrinogen. However, high
thrombin markers (fragments of prothrombin F1 + 2 and
thrombin-antithrombin complexes, TAT) indicate that th-
rombin is generated there. Thrombin substrates in loco
include protein C and pro-TAFI (procarboxipeptydase B);
the anticoagulant called activated protein C (APC) and
thrombin activatable fibrinolysis inhibitor (TAFI), a spe-
ctacular link between coagulation and fibrinolysis, are
formed there (for ref. see: [21]).
Moreover, the fluid contains other enzymatic systems
having cascade dynamics, which can generate pathoge-
nic substances, such as leukotrienes (arachidonic acid
cascade) and kinins (kallikrein-kinin cascade). Also all
proteins of the fibrinolytic system and products suggest-
ing plasmin activation are found there (for ref see: [22]).
2.4. The Thrombogenic Role of
Amniotic Cells
The majority of amniotic cells are derived from exfolia-
tion of squamous epithelium of the skin, from the mu-
cous membranes of the fetus (respiratory, digestive and
urinary tracts), the umbilical cord and the amnion [19].
During pregnancy, amniotic cells gradually and inevita-
bly go to apoptosis, gaining the properties of a particular
type of procoagulant (procoagulant-like activity).
The apoptotically altered amniotic cells harbor an
aminophospholipid called phosphatidylserine (PS) (ex-
ternalization from the inner layer of the cell membrane),
which has a negative charge and thus can accumulate on
the cell surface factors that become positively charged
when interacting with calcium ions (Ca2+), i.e. the fac-
tors necessary to the formation of thrombin. The proxi-
mity and the surface (the platform) create conditions for
the coagulation factors to interact. Thus, the interaction
of TF with VIIa yields a TF/VIIa complex at first, and
then a triple tenase complex of TF/VIIa/X, which in the
presence of calcium ions transforms the proenzyme,
prothrombin, into the active serine enzyme, thrombin.
Although the action of amniotic thrombin is restricted in
normal conditions to the amniotic fluid, in AFE amniotic
cells act as ready foci of DIC.
The role of amniotic cells in the generation of throm-
bin is a discovery which is the key to elucidate the
mechanism of DIC in amniotic fluid embolism [17]. Al-
ready in 1970, Slunsky [23], a Czech/Austrian author, in
his book on AFE noticed that amniotic cells were fre-
quently found inside microthrombi. We now consider it
to be the effect of thrombin formed on amniotic cells and
transforming fibrinogen into fibrin in its closest vicinity.
Here, a cell-based model of hemostasis proposed by
Hoffman and Monroe [24] in 2001 should be recalled.
According to this model, the surface of fibroblasts and
platelets constitutes a platform for the process of throm-
bin generation—first thrombin is produced in ignition
amounts (initiation of coagulation), followed by subse-
quent phases (amplification and propagation), in which
thrombin is generated in the amount able to produce a
hemostatic plug. The surface of amniotic cells can thus
have a similar role in the process of initiation of coagu-
lation as the surface of fibroblasts and blood platelets.
Amniotic cells seem to compensate for the lack of blood
platelets in amniotic fluid.
2.5. The Phenomenon of Pathogenic Potential of
Amniotic Fluid
Since the turn of the 1940s/50s there has been a dispute
attempting to elucidate whether the amount of TF in am-
niotic fluid embolism can elevate significantly TF con-
centration in the mother’s blood and whether this a-
mount can induce DIC. Researchers have varied in their
opinions in this field.
In 1957 Schneider [25] wrote: “Plausible as this at fir-
st seems, proof of significant release of thromboplastin
is still lacking”. In 1972 Phillips and Davidson [26] con-
cluded their research with the following: “The amount of
procoagulant …is probably insufficient to cause signify-
cant intravascular coagulation…”. A spectacular calcula-
tion by Mac Millan of 1968 [27] stated that the patho-
genic amount of TF could be found in 7 liters of the fluid,
whereas the volume of a genuine embolus was estimated
at 10 ml - 100 ml. Meta-analysis of my own study of
2003 [28] showed that TF contained in 100 ml super-
natant could cause only a statistically insignificant in-
crease in TF concentration in maternal blood (not ex-
ceeding standard deviation).
Despite these reservations, there can be a positive an-
swer to the question concerning the pathogenicity of am-
niotic TF. The following hypothesis can be proposed:
There are two TF fractions in amniotic fluid: 1) free
fraction found in the supernatant and 2) TF-cell bearing
(harboring) fraction, bound to the apoptosis-affected
amniotic cells. Only the TF fraction found on the surface
of amniotic cells can be ascribed the role of the initiator
of coagulation. These cells—after reaching pulmonary
arteries (amniotic embolism)—immediately become the
foci of fibrinogen transformation into fibrin (coagula-
tion), since they already have thrombin, an active serine
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M. Uszyński / Open Journal of Obstetrics and Gynecology 1 (2011) 178-183 181
enzyme, on their surface. On the other hand, the fraction
of “free TF”, i.e. TF found in the supernatant, does not
play a pathogenic role in amniotic fluid embolism.
Thus, the phenomenon of the thrombogenic potential
of amniotic fluid can be explained by integrated action
of three factors: 1) PS found on amniotic cells; 2) TF
and a few other coagulation factors that accumulate on
amniotic cells and form thrombin, and 3) the very am-
niotic cells which make a platform for thrombin genera-
tion.
3. NEW CLINICAL OBSERVATIONS
During the last 20 years some new, spectacular and ef-
fective diagnostic and therapeutic methods have been
described, which inspires revision of the common views.
This refers to e.g. the case of embolism after Cesarean
section reported by Esposito et al. in 1991 [29] and dur-
g Cesarean section described by Stanten et al. in 2003
[30]. In both cases, circulation arrest occurred and since
standard resuscitation procedure was ineffective, after
full heparinisation, cardiopulmonary bypass was insti-
tuted with a successful result. In the former case [29],
massive embolisation to the lung (pulmonary perfusion
scan) and embolus in the pulmonary artery with high
concentration of fetal squames (thromboembolectomy)
were detected, in the latter [30]—although the lumen of
the pulmonary arteries was free, transesophageal echo-
cardiogram showed catastrophic pulmonary vasoconstri-
ction. In both cases severe consumption coagulopathy was
observed.
These descriptions can be interpreted in the following
way: 1) disseminated intravascular coagulation (DIC)
takes place not only in pulmonary arterioles, but can also
reach the bifurcations and even the trunk of the pulmo-
nary artery, with fetal squamous cells and fibrin forming
“primary + secondary” embolic material (case 1); 2) two
pathogenic routes may exist alongside (catastrophic DIC
and catastrophic pulmonary vasoconstriction), and
therefore both routes should be considered during thera-
py (case 2); 3) full heparanisation was performed in car-
diopulmonary bypass procedure, which undoubtedly fa-
cilitated the maintenance and recovery of pulmonary va-
scular patency; 4) The process of DIC was already pre-
sent at the very beginning of the complication and if so,
only a targeted and immediate treatment could reduce
this process (pathogenetic treatment).
3.1. An Integrated Concept of Amniotic
Fluid Embolism
In the integrated concept of amniotic fluid embolism
(Figure 1), two amniotic fluid components, i.e. the apo-
ptosis-affected amniotic cells and leukotrienes play a role.
Figure 1. The mechanism of respiratory and circulatory disor-
ders in amniotic fluid embolism: two pathogenic pathways (A)
leading to catastrophic blockade of lung function (B), and cli-
nical sequels (C).
Each of these components induces different pathogenic
pathway (chain) in pulmonary vessels: 1) the apop-
tosis-affected cells become foci of thrombin, which leads
to DIC (DIC pathway); 2) leukotrienes and other me-
tabolites of arachidonic acid cascade, and possibly coex-
isting with them vasoactive substances, e.g. amniotic
endothelins, kinins and shock neurotransmitters, as well
as thrombin generated in the coagulation foci cause
catastrophic pulmonary vasoconstriction together with a
chain of sequels due to anoxia (the leukotriene pathway).
The obstruction of blood flow through the lungs is a
direct cause of cardio—pulmonary collapse. The blocka-
de occurs due to the following: 1) blood flow through
the lungs is hindered or blocked by amniotic cells and
amniotic debris found in pulmonary arteriolar circulation
(mechanical action per se); moreover, the blockade is
enhanced by secondary embolic material produced in the
process of DIC (fibrin accumulating around amniotic
cells); 2) pulmonary vasoconstriction caused by leukot-
rienes and/or other substances. Both types of disorders
have the same “onset time”.
3.2. Clinical Remark
In the light of the integrated concept of amniotic fluid
embolism, an old dilemma, i.e. indication for heparin
therapy in amniotic embolism, should be recalled. The
use of heparin or alternative medications (streptokinase,
recombinant tissue plasminogen activator, trasylol) should
be discussed and decided by appropriate scientific socie-
ties. “Full heparinization”—the management mentioned
in the casuistic reports cited can be indicated as a direc-
tion to follow. Literature reports on some signals con-
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cerning controlled heparin therapy in the first phase of
typical embolism (for ref. see: [31]).
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