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Amniotic Fluid Embolism 2012

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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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