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Amniotic Fluid Embolism
The E itome of the Obstetric Emer enc
Jeanne. S. Sheffield, M.D.
Maternal Fetal Medicine
University of Texas Southwestern
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I have no conflict of interest related
.
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Objectives
Review the diagnostic criteria for amnioticfluid embolism
Outline the potential etiologies for amniotic
Discuss the management of amniotic fluid
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Clinical Case Presentation
28 year old G2P1 hispanic female at 40
Prior CD for repeat CD Spinal anesthesia
Clear amniotic fluid
Female infant, 3165g Apgar score 9/9
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During placental removal (by fundal massage),
.
2 minutes later, while closing the incision of the
exteriorized uterus, she gasps, drops her oxygen
saturation to 57% becomes h otensive and
progresses to cardiopulmonary arrest.
Immediate intubation
Chest com ressions re uired for 4 minutes
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8 minutes after the initial arrest, 2 units ofwhole blood, 2 units of PRBCs and 2 units
of fresh frozen plasma are transfused
17 minutes after the initial arrest, moderateoozin is noted at the skin incision and IV
sites
PTT 45.4 sec
. . Hematocrit 36.2% and platelets 92,000/ul
rans erre o e or ven a or an
hemodynamic management
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Required an additional 2 units of PRBCs
Extubated 18 hours after the initial arrest
Discharged to home on hospital day 5
seemingly neurologically intact.
EMBOLISM?
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Amniotic Fluid Embolism
Initially described in 1926 by Meyer in the
-
Steiner and Luschbaugh in 1941 published acase series of maternal deaths, 8 of whom
had s uamous cells and mucin within the
maternal pulmonary vasculature. Of note,
a o er assoc a e agnoses.
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Hypotension
Hypoxia
Coagulopathy (forme fruste)
Reported incidence ranges from 1: 8,000 to
80 000 re nancies de endin on criteria used
Kramer 2012 2.5 per 100,000 deliveries (Canada)
,
Abenhaim 2008 7.7 per 100,000 deliveries (USA)
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0.5-1.7 deaths per 100,000 live births
5-15% of all maternal deaths in developed countries
Second highest cause of maternal death in the United States
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Proposed Risk Factors for AFE
Meconium stained amniotic fluid
Oxytocin ntrauter ne pressure cat eter nsert on
Male sex of the fetus
,
substantiated in the literature
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National Amniotic Fluid Embolism Registry
1988 a national registry was established to
Risk factors
n ca course
Pathophysiologic factors
Management
Published in 1995 b Clark et al
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tr ct entrance cr ter a
Acute hypotension and/or cardiac arrest
Acute hypoxia diagnosed by dyspnea, cyanosis
and/or respiratory arrest
Coagulopathy : intravascular consumption,
fibrinolysis and/or severe hemorrhage
Onset of the above during labor, cesarean delivery,
D and E or within 30 minutes ost artum
Absence of another etiology
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Study Population: National AFE Registry
46 women met the strict entrance criteria
19% AFE during cesarean delivery after
11% AFE immediately after a vaginal delivery
68% had the AFE within 5 minutes ofdelivery
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Risk Factors : The National AFE Registry
Male fetus 67% **
Uterine hyperstimulation 4%
econ um-sta ne
Hydramnios 5%
AROM/IUPC placement 14%
** Significant association
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AFE and MVA
1 case report of an AFE after bluntabdominal trauma inflicted in an MVA
? Seat belt positioning
pulmonary tissue (mast cell degranulation)
Rainio and Penttila For Sci Intern 11/2003
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Mode of Delivery
Deneux-Tharaux et al Obstet Gynecol
Survey No increase in AFE deaths with regards to
mode of delivery (vaginal versus Cesarean)
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Risk Factors for AFE in 2 large population-
ase co or s m on osp a e ver esKramer et al 2006 Abenhaim 2008
. . - . . . - .
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)orceps e very . . - . ) . . - . )
Vacuum delivery 2.9 (1.6-5.3) 1.9 (1.0-3.7)
Multi le re nanc 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)
Eclampsia 11.5 (2.8-46.9) 29.1 (7.1-119.3)
Fetal distress 1.7 (1.2-2.5) 1.5 (1.0-2.2)
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AFE has occurred after
Vaginal delivery Cesarean delivery
Transabdominalamniocentesis
Induced abortion
Feticide
Blunt abdominal
trauma Intrapartum
amnioinfusion
Surgical trauma
Removal of cerclage
Manual extraction ofthe placenta
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Pathophysiology of AFE
Conventional thinking defined the process, . .
forced amniotic fluid into the maternalcirculation. This fetal debri led to
obstruction of the pulmonary vasculature
with subsequent pulmonary hypertension
.
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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,
Myocardial Depression Pulmonary Hypertension DIC
, ,
ecrease ar ac u pu
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Pathophysiology: Cardiopulmonary
Few reports of initial severe pulmonary
ypertens on w t r g t eart a ure
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
-
intense vasoconstriction of pulmonary vasculature
All leading to profound hypoxia
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vasoconstriction and increased pulmonary
mechanisms responsible for cardiovascular
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Bick 2002
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Pathophysiology: National AFE Registry
Immunologic Role 41% women had a histor of dru aller or
atopy
Male fetus association
Hypersensitivity response
2001 Benson et al Markers for anaphylactoid
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How do you diagnose an AFE?
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Differential Diagnosis
Pulmonarythromboembolism
Placental abruption Peri artum
Transfusion reaction
Hemorrhage
cardiomyopathy
Eclampsia Air embolism
Ana h laxis
Myocardial infarction
Se tic shock
High spinal anesthesia Uterine rupture
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In the past, a definitive
dia nosis re uired
epithelial squamous
hairs or other fetal
pulmonary
m crovascu arcirculation
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73% fetal elements in the pulmonary
vascu ature
Requires special staining
Requires maternal death and/or pulmonary
Not sensitive nor specific
Current thinking : AFE is a clinical syndrome
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Clinical Findings in Amniotic Fluid Embolism
Clinical FindingsClark et al
n= 46Weiwen
n = 38
Hypotension 43 (94) 38 (100)
Fetal Distress
Pulmonary edema/ARDS28/30 11 (29)
Cardiopulmonary arrest
Cyanosis
40 (87)
38 (83)
38 (100)
38 (100)
CoagulopathyDyspnea
38 (83)22/45
12/1638 (100)
Seizure 22 (48) 6 (16)
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Classic Presentation of an AFE
Sudden cardiovascular collapse Profound s stemic h otension
Cardiac dysrhythmia
,
Pulmonary edema
Altered mental status Hemorrhage
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Clinical Findings in AFE
If survive the initial episode DIC
Multisystem organ failure
Neurologic dysfunction
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UK Confidential Inquiry into Maternal Deaths
Breathlessness
Lightheadedness
stress or pan c
Pins and needles in the fingers
Nausea and vomiting
11/17 women with an AFE
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Dia nosis:Laborator Evaluation
a diagnosis of exclusion. That being said
(DIC) evaluation
EKG may show tachycardia with RV
strainpattern
ABG: hypoxemia
WBCs ma be elevated
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Dia nosis:Laborator Evaluation
-
(Sialyl Tn fetal antigen)
component of fetal meconium
assuming an anaphylactoid pathophysiology
Serum insulin like growth factor binding
There is no test that can reliably confirm the diagnosis of an AFE
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Echocardiography
Case reports using TEE Normal left ventricular contractilit
Gross enlargement of the right ventricle and
main ulmonar 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
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Supportive care with the goal of maintaining
oxygenation and vital organ perfusion 100% su lemental ox en
Mechanical ventilation usually required
Optimize preload with volume replacement (isotonic
cr stalloid solution
Inotropic agents to improve myocardial function
Pulmonary artery catheter useful
? Cardiopulmonary bypass
?ECMO
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ACUTE RESPIRATORY DISTRESS SYNDROME
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anagemen o
Blood component therapy
FFP versus Cryoprecipitate depending on volume
needs
Recombinant Factor VIIa
Aprotinin and serine proteinase inhibitor FOY
Annecke et al algorithm based coagulationmanagement 2010
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Recombinant Factor V11a
Case reports using recombinant factor V11ato successfull mana e DIC from an AFE
Given 2 hours post-op when coagulopathy
ersisted with a ressive blood roductreplacement
Stated bleeding improved within 10 minutes and lab
values improved within 2 hours of injection
Lim et al Int J Obstet Gyn 2004 87: 178-179
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Systemic Review
Recombinant factor VIIa cases hadsi nificantl worse outcomes than cohorts
who did not receive rVIIa
hemorrhage cannot be stopped by massive
Leighton et al Anesthesiology 2011 115:1201-1208
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Clark et al 1995
neurologic damage
Dismal outcomes independent of clinical setting and
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Maternal Outcomes: United Kingdom AFE
Registry
Tuffnell DJ 2005
7% of survivors remaining neurologically
mpa re
Knight et al 2010
20% case fatality rate
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Gilbert et al 1999
1.1 million women delivering at a California acutecare 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 mortalit 22%
Roberts et al Australia 2010
Kramer et al UK 2012 27% case fatality rate
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Amniotic Fluid Embolism
Catastrophicnpre c a e
Unpreventable? Untreatable
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