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Amniotic Fluid Embolism

Thee Epitome
p o e of
o thee Obstetric
Obs e c Emergency
e ge cy
Jeanne. S. Sheffield, M.D.
Maternal Fetal Medicine
University of Texas Southwestern
Medical Center

I have no conflict of interest related


to the content of this presentation.
presentation

Amniotic Fluid Embolism


Objectives
Review the diagnostic criteria for amniotic
fluid embolism
Outline the potential etiologies for amniotic
fluid embolism
Discuss the management of amniotic fluid
embolism

Clinical Case Presentation


28 year old G2P1 hispanic female at 40
weeks gestation presents in early labor
Prior CD for repeat CD
Spinal anesthesia
Clear amniotic fluid
Female infant, 3165g Apgar score 9/9

During placental removal (by fundal massage),


she begins to cough intermittently
intermittently.
2 minutes later, while closing the incision of the
exteriorized uterus, she gasps, drops her oxygen
saturation
sa
u a o too 57% , becomes
beco es hypotensive
ypo e s ve aand
d
progresses to cardiopulmonary arrest.
Immediate intubation
p
required
q
for 4 minutes
Chest compressions

8 minutes after the initial arrest, 2 units of


whole blood, 2 units of PRBCs and 2 units
of fresh frozen plasma are transfused
17 minutes after the initial arrest, moderate
oozing is noted at the skin incision and IV
sites

Fibrinogen 147 mg/dL


PTT 45.4 sec
PT 11
11.9
9 sec INR 1.0
10
Hematocrit 36.2% and platelets 92,000/ul

T
Transferred
f
d to
t the
th SICU for
f ventilator
til t andd
hemodynamic management

Required an additional 2 units of PRBCs


and 4 units of FFP
Extubated 18 hours after the initial arrest
Discharged to home on hospital day 5
seemingly neurologically intact.
DID SHE HAVE AN AMNIOTIC FLUID
EMBOLISM?

Amniotic Fluid Embolism


Initially described in 1926 by Meyer in the
Brasil Medica
Brasil-Medica
Steiner and Luschbaugh in 1941 published a
case series of maternal deaths, 8 of whom
had squamous cells and mucin within the
maternal pulmonary vasculature. Of note,
7/8 had
h d other
th associated
i t d diagnoses.
di

Amniotic Fluid Embolism


Traditionally described using a diagnostic
diagnostic triad
triad
Hypotension
Hypoxia
i
Coagulopathy (forme fruste)

Reported incidence ranges from 1: 8,000 to


80,000
,
ppregnancies
g
depending
p
g on criteria used
Kramer 2012 2.5 per 100,000 deliveries (Canada)
Knight 2010 2 per 100
100,000
000 deliveries (UK)
Abenhaim 2008 7.7 per 100,000 deliveries (USA)

Amniotic Fluid Embolism


One of the leading causes of maternal death
0.5-1.7 deaths per 100,000 live births
5-15%
1 % off all
ll maternall deaths
d h in
i developed
d l d countries
i
Second highest cause of maternal death in the United States

Proposed Risk Factors for AFE

Meconium stained amniotic fluid


Precipitous labor
Oxytocin
I
Intrauterine
i pressure catheter
h
insertion
i
i
Male sex of the fetus
However, no risk factor has been consistently
However
substantiated in the literature

National Amniotic Fluid Embolism Registry


1988 a national registry was established to
help define the following
Risk factors
Clinical
Cli i l course
Pathophysiologic factors
Management

Published in 1995 by
y Clark et al

National Amniotic Fluid Embolism Registry


Strict
S i entrance criteria
i i
Acute hypotension and/or cardiac arrest
Acute hypoxia diagnosed by dyspnea, cyanosis
and/or respiratory arrest
Coagulopathy : intravascular consumption,
y and/or severe hemorrhage
g
fibrinolysis
Onset of the above during labor, cesarean delivery,
p
D and E,, or within 30 minutes ppostpartum
Absence of another etiology

Study Population: National AFE Registry


46 women met the strict entrance criteria
70%

AFE during labor

19%

AFE during cesarean delivery after


delivery of the infant

11%

AFE immediately after a vaginal delivery

68% had the AFE within 5 minutes of


delivery

Risk Factors : The National AFE Registry

Male fetus
Oxytocin
Uterine hyperstimulation
M
Meconium-stained
i
i d AF
Hydramnios
AROM/IUPC placement

** Significant association

67% **
50%
4%
19%
5%
14%

AFE and MVA


1 case report of an AFE after blunt
abdominal trauma inflicted in an MVA
? Seat belt positioning
Positive IHC staining for antitryptase in
pulmonary tissue (mast cell degranulation)
Rainio and Penttila For Sci Intern 11/2003

Maternal Mortality from AFE :


Mode of Delivery
Deneux-Tharaux et al Obstet Gynecol
2006; 108:541 French National Perinatal
Survey
No increase in AFE deaths with regards to
mode of delivery (vaginal versus Cesarean)

Risk Factors for AFE in 2 large populationbased cohorts (3 million hospital deliveries)
Kramer et al 2006

Abenhaim 2008

Maternal age <20 years

0 2 (0.1-0.96)
0.2
(0 1 0 96)

0 4 (0.2-0.9)
0.4
(0 2 0 9)

Maternal age 35 years

1.9 (1.4-2.7)

2.2 (1.5-2.1)

Previous cesarean

0.8 (0.5-1.2)

0.9 (0.6-1.3)

Medical induction labor

1.8 (1.3-2.7)

-----

Cesarean delivery

12.5 (7.9-19.9)

5.7 (3.7-8.7)

F
Forceps
delivery
d li

5 9 (3.4-10.3)
5.9
(3 4 10 3)

4 3 (1.9-6.6)
4.3
(1 9 6 6)

Vacuum delivery

2.9 (1.6-5.3)

1.9 (1.0-3.7)

Multiple
p ppregnancy
g
y

2.5 ((0.9-6.2))

1.5 ((0.6-4.1))

Placenta previa/abruption

3.5 (2.3-5.5)

-----

Preeclampsia

1.4 (0.8-2.5)

7.3 (4.3-12.5)

11.5 (2.8-46.9)

29.1 (7.1-119.3)

1.7 (1.2-2.5)

1.5 (1.0-2.2)

Eclampsia
Fetal distress

AFE has occurred after

Vaginal delivery
Cesarean delivery
Induced abortion
Feticide
Intrapartum
amnioinfusion
Manual extraction of
the placenta

Transabdominal
amniocentesis
Blunt abdominal
trauma
Surgical trauma
Removal of cerclage

Pathophysiology of AFE
Conventional thinking defined the process
as an event
event, ii.e.
e tetanic contraction that
forced amniotic fluid into the maternal
circulation. This fetal debri led to
obstruction of the pulmonary vasculature
with subsequent pulmonary hypertension
and eventually acute cor pulmonale.
pulmonale

Pathophysiology: Contemporary
Thinking
Foreign Substance Enters the Maternal Circulation
(Common)

Small % of Women anaphlylactoid reaction versus complement activation versus ????

Release of Endogenous Mediators


Thromboxane, histamine, bradykinin, cytokines,
prostaglandins leukotrienes,
prostaglandins,
leukotrienes endothelin

Myocardial Depression
Decreased Cardiac Output

Pulmonary Hypertension

DIC

Pathophysiology: Cardiopulmonary
Few reports of initial severe pulmonary
h
hypertension
i with
i h right
i h heart
h
failure
f il
Followed by an increase in PCWP with left
ventricular dysfunction and a decreased LV
stroke-work index leading to pulmonary edema
Decrease also in systemic vascular resistance
Severe ventilation
ventilation-perfusion
perfusion mismatch due to
intense vasoconstriction of pulmonary vasculature
All leading to profound hypoxia

Pathophysiology: Cardiopulmonary
These findings suggest that pulmonary
vasoconstriction and increased pulmonary
vascular resistance are the primary
mechanisms responsible for cardiovascular
collapse

Pathophysiology: Coagulopathy

Bick 2002

Pathophysiology: National AFE Registry


Immunologic Role
41% women had a history of drug allergy or
atopy
Male fetus association
Hypersensitivity response

Mast cell degranulation in question


2001 Benson et al Markers for anaphylactoid
reaction (sialyl Tn)

How do you diagnose an AFE?

Differential Diagnosis
Pulmonary
thromboembolism
Transfusion reaction
Hemorrhage
Air embolism
p y
Anaphylaxis
High spinal anesthesia

Placental abruption
p
Peripartum
cardiomyopathy
Eclampsia
Myocardial infarction
Septic
p shock
Uterine rupture

In the past, a definitive


diagnosis
g
required
q
epithelial squamous
cells, mucin, lanugo
hairs or other fetal
debri in the maternal
pulmonary
microvascular
i
l
circulation

Diagnosis: National AFE Registry


22 women underwent an autopsy
73% fetal elements in the pulmonary
vasculature
l t

Requires special staining


Requires maternal death and/or pulmonary
vessel or right heart aspiration
Not sensitive nor specific
Current thinking : AFE is a clinical syndrome

Clinical Findings in Amniotic Fluid Embolism


Clinical Findings
Hypotension
Fetal Distress
Pulmonary edema/ARDS
Cardiopulmonary arrest
Cyanosis
Coagulopathy
Dyspnea
Seizure

Clark et al
n= 46

Weiwen
n = 38

43 (94)
30/30
28/30
40 (87)
38 (83)
38 (83)
22/45
22 (48)

38 (100)
NS
11 (29)
38 (100)
38 (100)
12/16
38 (100)
6 (16)

Classic Presentation of an AFE


Sudden cardiovascular collapse
Profound systemic hypotension
Cardiac dysrhythmia

Cyanosis, dyspnea or respiratory arrest


Cyanosis
Pulmonary edema
Altered mental status
Hemorrhage

Clinical Findings in AFE


If survive the initial episode

DIC
Multisystem organ failure
ARDS
Neurologic dysfunction

?? Premonitory Symptoms
UK Confidential Inquiry into Maternal Deaths

Breathlessness
Chest pain
Lightheadedness
Di
Distress
or panic
i
Pins and needles in the fingers
Nausea and vomiting
Feeling cold
11/17 women with an AFE

Diagnosis:Laboratory Evaluation
AFE is based on clinical presentation and is
a diagnosis of exclusion. That being said
Disseminated Intravascular Coagulopathy
(DIC) evaluation
Cardiac enzymes may be elevated
EKG may show tachycardia with RV
strainpattern

ABG: hypoxemia
WBCs may
y be elevated

Diagnosis:Laboratory Evaluation
TKH-2
TKH 2 monoclonal antibody to fetal mucin
(Sialyl Tn fetal antigen)
Maternal zinc coproporphyrin I
component of fetal meconium

Tryptase levels
assuming an anaphylactoid pathophysiology

Decreased complement levels (C3 and C4)


Serum insulin like growth factor binding
protein 1
There is no test that can reliably confirm the diagnosis of an AFE

Diagnosis: Transesophageal
Echocardiography
Case reports using TEE
Normal left ventricular contractility
Gross enlargement of the right ventricle and
main ppulmonary
y tree
Acute right ventricular pressure overload
Underloading of the left ventricle due to pulmonary
vasoconstriction
James CF et al. Int J Ob Anesth 13:279-83,, 2004
Stanten RD et al. Obst Gyn 102:496-498, 2003
McDonnell et al Int J Obstet Anesth 16:269-73, 2007

Management of AFE
Supportive care with the goal of maintaining
oxygenation and vital organ perfusion
100% supplemental
pp
oxygen
yg
Mechanical ventilation usually required

Maintain cardiac output and blood pressure


Optimize preload with volume replacement (isotonic
crystalloid
y
solution))
Inotropic agents to improve myocardial function
Pulmonary artery catheter useful
? Cardiopulmonary bypass
?ECMO

ACUTE RESPIRATORY DISTRESS SYNDROME

Management of AFE
Combat the severe coagulopathy
Blood component therapy
FFP versus Cryoprecipitate
C
i i
depending
d
di on volume
l
needs
Recombinant Factor VIIa
Aprotinin and serine proteinase inhibitor FOY
Annecke et al algorithm based coagulation
management 2010

Recombinant Factor V11a


Case reports using recombinant factor V11a
to successfully
y manage
g DIC from an AFE
Given 2 hours post-op when coagulopathy
ppersisted with aggressive
gg
blood product
p
replacement
Stated bleeding improved within 10 minutes and lab
values
l
improved
i
d within
i hi 2 hours
h
off injection
i j i
Prosper et al Obstet and Gynecol 2007; 109:524
Lim et al Int J Obstet Gyn 2004 87: 178-179

Recombinant Factor VIIa


Systemic Review
Recombinant factor VIIa cases had
significantly
g
y worse outcomes than cohorts
who did not receive rVIIa
Use only in AFE patients when the
hemorrhage cannot be stopped by massive
blood component replacement

Leighton et al Anesthesiology 2011 115:1201-1208

Maternal Outcomes: National AFE Registry


Clark et al 1995
85% of the women either died or had permanent
neurologic damage
61% maternal mortality
Dismal outcomes independent of clinical setting and
treatment rendered

Maternal Outcomes: United Kingdom


g
AFE
Registry

Tuffnell DJ 2005
37% maternal mortality
7% of survivors remaining neurologically
i
impaired
i d

Knight et al 2010
20% case fatality rate

Maternal Outcomes
Gilbert et al 1999
1.1 million women delivering at a California acute
care civilian hospital over a 2 year period
53 cases with a maternal mortality rate of 26.4%

Burrows and Khoo 1995


10 cases of AFE
Maternal mortalityy 22%

Roberts et al Australia 2010


35% case fatality rate

Kramer et al UK 2012 27% case fatality rate

Amniotic Fluid Embolism


Catastrophic
U
Unpredictable
di t bl
p
Unpreventable
? Untreatable