Amniotic Fluid Embolism 2012

8/10/2019 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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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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Catastrophicnpre c a e

Unpreventable? Untreatable

Documents

Amniotic Fluid Embolism 2012