Clinical Expert Series
Amniotic Fluid Embolism
Steven L. Clark, MD
Obstet Gynecol 2014;123:337–48
Continuing Medical Education credit is provided through joint sponsorship with
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Before submitting this form, please print a completed copy as confirmation of your program participation.
College Fellows: To obtain credits, complete and return this form by e-mail (obgyn@greenjournal.org) or fax (202-479-0830).
Your score, and a copy of the answer key, will be e-mailed to you after receipt of a completed quiz. Credit will be recorded for
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Non–College Fellows: To obtain credits, submit the printout of the completed quiz to your accrediting institution. The printout of
the completed quiz is documentation for your continuing medical education credits.
Continuing medical education credit for “Amniotic Fluid Embolism” will be available through February 2017.
1. The pathophysiology of amniotic fluid embolism appears to involve:
Release of fetal platelet prostaglandins
An abnormal maternal response to fetal tissue exposure
Uterine oxytocin release
Mechanical obstruction of maternal coronary microvasculature
Down-regulation of the classic systemic inflammatory response
CME Quiz for the Clinical Expert Series
Obstet Gynecol 2014;123(2)
Credit available through February 2017
Page 1 of 3
2. Clinical series or amniotic fluid embolism cases based on population or administrative databases that
do not include individual chart review by individuals with expertise in critical care obstetrics are
likely to:
Underestimate incidence
Underestimate mortality
Underestimate prevalence
Overestimate negative predictive value
Overestimate clinical severity
3. Fetal antigens enter the maternal circulation:
Only in cases of occult uterine rupture
Primarily in cases of manual removal of the placenta
Only when there is separation of the placenta before fetal delivery
Only in cases of operative vaginal or abdominal delivery
In nearly all deliveries
4. The factor that seems to predict the severity of findings in patients with amniotic fluid embolism is
the:
Nature of the inciting antigen
Degree of abnormal host response
Volume of fluid entering the maternal circulation
Amount of cellular debris transfused
Stage of labor when the event occurs
5. Future efforts to prevent amniotic fluid embolism may rely upon:
Reduced use of oxytocin
Identification of women at risk
Increased use of prostanoids during labor
Cesarean delivery in selected cases
Routine rupture of the membranes early in labor
6. If the fetus is in utero at the onset of amniotic fluid embolism syndrome, the most typical fetal heart
rate manifestations are:
Tachycardia
Acute, prolonged decelerations
Increased variability
Sinusoidal fluctuations
Early pattern decelerations
CME Quiz for the Clinical Expert Series
Obstet Gynecol 2014;123(2)
Credit available through February 2017
Page 2 of 3
7. The diagnosis of amniotic fluid embolism is primarily based on finding:
Fetal squamous cells in maternal circulation
Sudden hypoxia, hypotension, and coagulopathy
Defects or missing cotyledons upon inspection of the placenta
Elevated maternal serum C-reactive protein
Reduced or absent amniotic fluid volume
8. Effective treatment of amniotic fluid embolism is based on observable pathophysiology and:
Early administration of anti-prostaglandin agents
Uterine tocolytics
Fluid restriction
Exchange transfusions
Supportive measures
9. In patients with amniotic fluid embolism and maternal cardiac arrest, prompt delivery of the fetus
results in:
Improved maternal survival
Improved likelihood of a good newborn outcome
Reduced rates of maternal coagulopathy
Reduced maternal oxygen demand
Increased risk of right heart failure
10. Based on our current understanding of amniotic fluid embolism syndrome, the most likely cause is:
Fetal platelet aggregation
Trophoblastic-derived antigens
Mechanical vascular obstruction
HLA-mediated cellular rejection
Maternal red cell lysis
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CME Quiz for the Clinical Expert Series
Obstet Gynecol 2014;123(2)
Credit available through February 2017
Page 3 of 3