PREECLAMPSIA:
“Behind the Scenes”
MATERNAL AND FETAL
PATHOPHYSIOLOGIC
IMPLICATIONS
Alverno College-MSN 621
May 2006
Nancy Rogers RNC BSN
Leslie Dittus-Yaeger RNC BSN
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Intended Audience
This tutorial is intended for experienced Labor
and Delivery nurses with a working knowledge
of the nursing care of a preeclamptic patient.
It is intended to provide an in depth look at the
pathophysiology of the disease process, review
some current research and discuss future
implications.
If you would like additional information about the
medical diagnosis and treatment of
preeclampsia, please click on the link below:
(use the “back” button on your browser to return to the tutorial)
http://www.emedicine.com/med/topic1905.htm
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Tutorial Objectives
Review a two stage model of the pathophysiologic
changes associated with preeclampsia.
Explore possible theories that link the development
of maternal disease from the fetal beginnings.
Recognize why diverse manifestations of the
disease process are possible.
Review the fetal effects of the maternal disease
process.
Discuss future implications of current research.
Participate in a fetal monitor strip review of a patient
diagnosed with preeclampsia.
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Preeclampsia is a pregnancy
complication recognized by:
New-onset gestational hypertension
systolic >140mm Hg
or diastolic >90mm Hg
Proteinuria (>300 grams in 24 hours)
Preeclampsia affects both mothers and
their infants.
Preeclampsia is cured only by delivery.
Induction of labor to prevent the progression of
preeclampsia is responsible for 15% of preterm births.
Early identification and intervention via delivery has
changed little in 100 years.
What have we learned about preeclampsia?
Let’s explore current theories related to the
pathophysiology involved in preeclampsia.
Microsoft Office 2000
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Two-stage model of the pathophysiology of
preeclampsia
Roberts, J. M. et al. Hypertension 2005;46:12431249
Used with permission
Stage 2 develops in
some, but not all
women with stage 1
Copyright ©2005 American Heart Association
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DEVELOPMENT OF
STAGE 1
Poor placentation
Normal Placental Development
From 9-12 weeks
gestation the uterine
spiral arteries are
transformed from thickwalled, muscular vessels,
to more flaccid tubes to
accommodate a 10-fold
increase in uterine blood
flow to support the
pregnancy.
Uterine spiral
Uterine spiral
arteries
arteries
C. W. Redman et al., Science 308, 1592 -1594 (2005)
Used with permission
National Institute of Health (NIH) National High Blood Pressure
Education Program Working Group on High Blood Pressure in
Pregnancy, (2000)
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Normal Placental Development
Uterine spiral artery remodeling takes
place by the invasion of trophoblast cells
into the uterine lining.
These trophoblasts enter the arterial walls
and replace parts of the vascular
endothelium so that smooth muscle is lost
and the artery dilates.
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An immune response facilitates
normal placental development:
In the uterine decidua, maternal
lymphocytes and macrophages assist the
trophoblasts to invade into the uterine
myometrium and the spiral arteries.
Redman, C.W., Sargent, I.L. (2005)
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Placental Pathophysiology in
Stage 1
Trophoblasts fail to completely remodel
the uterine spiral arteries.


Remodeling either absent
or
Remodeling limited to the superficial portion
of the artery located in the decidua, rather
than extending into the inner third of the
myometrium.
Redman, C.W., Sargent, I.L. (2005)
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Theoretical basis for incomplete
remodeling:


Production failure of endothelial adhesion
molecules from trophoblasts
or
Failure of/ or weak signaling of immune cells
by trophoblasts prevents deep invasion
necessary for normal artery remodeling.
(NIH 2000)
Redman, C.W., Sargent, I.L .(2005)
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Poor placentation and preeclampsia
C. W. Redman et al., Science 308, 1592 -1594 (2005)
Used with permission
Uterine spiral artery
“unwinds” and becomes
a wider, flaccid tube to
accommodate increased
blood flow.
Uterine spiral artery
remains tightly coiled,
diminishing placental
blood flow
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THE RESULT:
Poor placentation, or a decreased capacity
of the uteroplacental circulation. This
causes placental hypoxia, resulting in
oxidative stress.

Pathophysiology is generally established
before 20 weeks.
(NIH, 2000)
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DEVELOPMENT OF
STAGE 2
Evidence of Maternal Disease
Process
View previous slide
The beginnings of the maternal
disease process:
Stage 2 begins when maternal clinical
features appear.


Cause is most likely related to the hypoxic
and dysfunctional placenta releasing factors
into the maternal circulation resulting from cell
death.
These factors target the maternal
endothelium, causing vascular damage.
Roberts, J.M., Gammill H.S. (2005)
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Stage 2:
Multisystemic, maternal syndrome
Perfusion is
reduced to
virtually every
organ
Reduced uterine
blood flow
Reduced
Placental
perfusion
Release of
ToxinsMaternal
Endothelial
damage
Roberts, J.M., Gammill H.S. (2005)
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Normal function of endothelial cells
Line all blood vessels providing vessel wall
integrity
Prevent intravascular coagulation
Regulate smooth muscle contractility
Mediate immune and inflammatory
responses
Gilbert E.S., & Harmon J.S. (2003). Hypertensive Disorders. In Manual of High Risk Pregnancy
and Delivery ( p. 451). St Louis, MO: Mosby.
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Toxic factors released by the placenta
are believed to cause maternal
endothelial dysfunction by one or more
of following mechanisms:
1. The factors are directly toxic to endothelial
cells
2. The factors stimulate maternal oxidative
stress
3. The factors stimulate/activate
inflammatory cytokines
Roberts, J.M., Gammill H.S. (2005)
Gilbert & Harmon (2003) p. 451
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Oxidative stress is the imbalance of:
Pro-oxidants:
Homocysteine
LDL
Hypertriglyceridemia
Increased iron
Antioxidants:
HDL
transferrin, a
blood protein
which binds with
iron
Gilbert & Harmon (2003) p. 451
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Oxidative stress may be the
mechanism causing endothelial
dysfunction:
leads to the formation of oxygen
free radicals and lipid peroxides
free radicals are highly reactive,
interacting with and damaging molecules
within the cells
lipid peroxides and free radicals are both
directly toxic to endothelial cells
Gilbert & Harmon (2003) p. 451
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Increasing the inflammatory
response/activating cytokines may be
the mechanism causing endothelial
dysfunction:
Cytokines cause the additional release of
free radicals, fueling the oxidative stress
response
Cytokines directly damage the endothelial
cells lining maternal blood vessel walls
Roberts, J.M., Gammill H.S. (2005)
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With maternal endothelial damage:
Decreased
production of
vasodilators
(prostacyclin and
nitric oxide)
Inactivation of
circulating nitric
oxide (vasodilator).
Poor tissue perfusion
to all maternal organs
VASOSPASM
Increases total
peripheral resistance
resulting in
elevated blood pressure
Gilbert & Harmon (2003) pp. 451-452
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Maternal vasospasm also causes:
Increases endothelial cell permeability,
(“leaky capillaries”) fluid shifts from
intravascular to intracellular space
resulting in:


Decreased plasma volume, increased
hematocrit
Generalized tissue and organ edema
Gilbert & Harmon (2003) pp. 451-452
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Additionally, damage to the
vascular endothelium causes:
Increased production of thromboxane
which leads to clot formation through
increasing platelet adhesion.
Activation of the clotting cascade
Decreased production of platelets
Gilbert & Harmon (2003) pp. 451-452
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Putting theory into practice:
In a preeclamptic patient, clinical
“evidence” of vasospasm may include:
Click on each correct answer, more than one may be correct!
1. Generalized edema
2. Kidney dysfunction, proteinuria
3. Elevated blood pressure
Click here to continue with presentation
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Correct!
Vasospasm of maternal blood vessels causes
damage to endothelial cells, causing them to
become more permeable.
Fluid “leaks” out of the blood vessels into the
tissues, causing tissue and organ edema
Normal physiological edema in pregnancy
should disappear after 8-12 hours of bedrest.
This does not happen in preeclampsia.
However, the effects of vasospasm are not
confined to edema…
Click on view previous slide
button to return to question for
more information on vasospasm.

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Correct!
Vasospasm causes poor tissue perfusion to all
organs, leading to organ dysfunction.
Decreased perfusion to the kidney results in
decreased glomerular filtration, allowing protein,
mainly albumin, to be lost into the urine.
Oliguria develops as the disease worsens.
Vasospasm is evident in other clinical signs…
Click on view previous slide
button to return to question for
more information on vasospasm.

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Correct!
Vasospasm and endothelial damage upset
the delicate balance between
vasoconstrictors and vasodilators.
This imbalance causes generalized
vasoconstriction, which increases
peripheral vascular resistance, resulting in
hypertension.
The results of vasospasm are not confined to elevated
blood pressure…
Click on view previous slide
button to return to question for
more information on vasospasm

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If you selected all three options, you
have successfully integrated theory
and practice!
In summary, maternal endothelial damage
causes vasospasm.
Vasospasm causes:



Leaky capillaries resulting in tissue and organ edema
Poor tissue perfusion to all maternal organs, resulting
in organ dysfunction
Increased peripheral resistance resulting in elevated
blood pressure
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Additional clinical findings of preeclampsia
include: visual disturbances, headache,
and hyperreflexia.
Headache and hyperreflexia are caused
by cerebral edema.
Endothelial damage in the brain may lead
to cerebral hemorrhage and seizure
activity.
Visual disturbances are caused by
vasospasms of retinal blood vessels.
Vasospasms may affect all maternal blood
vessels…
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WHAT LINKS STAGE
1 & 2?
Theory exploration:
Genetics/Abnormal lipid metabolism
Endocrine dysfunction
Inflammation
Not all women with reduced placental
perfusion develop preeclampsia…
What links stages 1 and 2?
Stage 1
???
Stage 2
Reduced placental perfusion must interact
with maternal factors to result in
preeclampsia.
Roberts, J.M., Gammill H.S. (2005)
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Diverse manifestations are possible:
maternal and fetal/placental factors may
vary in proportion.
In a woman with many predisposing factors, even a
minor reduction in placental perfusion is sufficient for
stage 2 to develop.
In a woman with few predisposing factors, a profound
reduction in placental perfusion may be required for
preeclampsia to develop.
Reduced placental
perfusion
Predisposing
factors
Microsoft Office 2000
Roberts, J.M., Gammill H.S. (2005)
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Could maternal genetics play a role in
the link between stage 1 & 2?
Stage 1
Genetics
Stage 2
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What do we know?
We know that abnormalities in lipid
metabolism have a genetic basis.
We have learned that preeclampsia is
characterized by profound lipid
abnormalities such as
hypertriglyceridemia…
Gratacos, E. (2000)
Microsoft Office 2000
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Could abnormal lipid metabolism
be a genetic factor linking the
stages of preeclampsia?
Stage 1
Abnormal lipid
metabolism
Stage 2
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Preeclampsia is characterized by
metabolic abnormalities similar to those
present in atherosclerosis:
Hypertriglyceridemia
Reduced HDL cholesterol
Predominance of small-dense LDL
cholesterol which have an increased
potential to cause endothelial cell
damage as compared to larger, more
buoyant LDL’s.
Gratacos E., 2000.
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In the presence of oxidative stress and
inflammation, susceptible small-dense
lipoproteins may be more easily
oxidized, triggering Stage 2, maternal
disease.
Stage 1
Abnormal lipid metabolism
+ Oxidative Stress
Stage 2
+ Inflammation
Gratacos E., 2000
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Most of the suggested linkages could
contribute to or be stimulated by oxidative
stress.
Oxidative stress is proposed as relevant to many diseases.
Evidence supports the presence of oxidative stress in
preeclampsia:
Protein products of oxidative stress present in maternal
and fetal tissues
Antibodies to oxidatively modified LDL’s present in
maternal and fetal tissues
Concentrations of certain antioxidants reduced in
preeclamptic women.
Roberts, J.M., Gammill H.S. (2005)
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In summary:
Hypertriglyceridemia and predominance of
small-dense LDL’s prior to pregnancy could
be one predisposing factor for developing
preeclampsia.
Oxidative stress and inflammation
may trigger the maternal disease.
Gratacos E., (2000)
Microsoft Office 2000
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Could endocrine dysfunction be a
factor linking Stage 1 and Stage 2?
Stage 1
Endocrine dysfunction
Stage 2
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There is growing evidence suggesting that
preeclampsia may be an early manifestation of
the “metabolic syndrome”:
elevated triglyceride levels
hyperinsulinemia
insulin resistance
relative glucose intolerance
elevated blood pressure
These factors have been linked to the
development of preeclampsia.
Innes, K., Weitzel, L., Laudenslager, M. (2005)
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Studies have repeatedly demonstrated that
metabolic abnormalities precede the clinical
signs of preeclampsia:
Insulin resistance and associated
hyperinsulinemia
Glucose intolerance
Hypertriglyceridemia
This suggests that insulin resistance and
dyslipidemia may be factors involved in
the development of preeclampsia.
Innes, et al. (2005)
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Similarities between the risk factors for
preeclampsia and cardiovascular disease
include:
Insulin resistance
Dyslipidemia- decreased HDL levels and
elevated triglyceride levels
These risk factors are thought to play a causal role
in the development of endothelial dysfunction, a
characteristic feature of preeclampsia and
cardiovascular disease.
Innes, et al. (2005)
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Future implications:
Studies have demonstrated that women with a history of
preeclampsia are at increased risk of developing cardiovascular
disorders later in life.
Women with preeclampsia who deliver preterm or with recurrent
preeclampsia are at greatest risk.
Women with preeclampsia have an approximate doubling of risk
death from cardiovascular disease.
These findings suggest that pregnancy may constitute a metabolic
and vascular stress test which reveals a woman’s health in later life.
Identification of maternal factors provides specific targets for
prevention of preeclampsia in “at-risk” women.
Innes, et al. (2005)
Roberts, J.M., Gammill H.S. (2005)
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Could inflammation be a factor linking
Stage 1 and Stage 2?
Stage 1
Inflammation
Stage 2
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“Preeclampsia is associated with an
excessive inflammatory response
compared with normal pregnancy.”
In a study done by Braekke, et.al (2005)
inflammatory markers (calprotectin, CRP)
were evaluated in maternal and fetal
serum and amniotic fluid.
Braekke, K., Holthe, Ml, Harsem, N., Fagerhol, M., Staff, A., 2005
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Inflammatory Markers:
Calprotectin:
Is a protein released
by activated
neutrophils
C-reactive protein (CRP):
Is a protein produced by the
liver
Production is stimulated by
inflammatory cytokines
Braekke, K. et. al. (2005)
Microsoft Office 2000
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Calprotectin and C-reactive protein
(CRP), markers of inflammation, are
elevated in preeclampsia.
The concentration of calprotectin in the
maternal plasma of preeclamptic women
was higher than in the control group
(normal pregnant women).
No statistically significant difference in
calprotectin levels was noted between
women with mild and severe preeclampsia
Braekke, K. et al. (2005)
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C-reactive protein:
Has been used to evaluate low-grade
inflammation as a cardiovascular risk factor
Braekke et al. 2005
Microsoft Office 2000
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CRP levels in the maternal plasma of
pregnant women:
Correspond to a low-grade inflammation
in preeclampsia and in normal pregnancy.
Braekke et al. 2005
Microsoft Office 2000
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No inflammatory response was noted in
the fetal circulation.
Concentrations of calprotectin in both
arterial and venous umbilical plasma, and
amniotic fluid were much lower than in
maternal plasma
CRP levels in fetal circulation were 1/100
of maternal CRP levels.
Braekke et al. 2005
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Theoretically,
“Calprotectin concentrations could play a
role in the pathophysiology of
preeclampsia through augmented
placental cell death or reduced trophoblast
invasion (stage 1)”
Braekke et al. 2005
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What stimulates the inflammatory
response (activates the neutrophils) in
preeclampsia?
Researchers have been unable to determine
why or exactly where the neutrophils become
activated.
Maternal or placenta factors triggering maternal
inflammation do not appear to be transferred
into the fetal circulation.
Braekke et al. 2005
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Future implications:
Further research is needed to evaluate the
role of calprotectin in pregnancy or
pregnancy complications.
Will calprotectin concentrations be used
to predict preeclampsia before the onset of
clinical symptoms or as a marker of the
clinically established disease?
Braekke et al. 2005
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INHERITANCE PATTERNS
AND CULTURAL
CONSIDERATIONS
What has research told us about
inheritance patterns in preeclampsia?
Preeclampsia is clearly inherited, but
does not depend on a single maternal or
fetal gene.
Studies support a multifactorial
inheritance.
Roberts, J., Gammill, H. (2005)
Microsoft Office 2000
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The role of ethnicity in the expression
of preeclampsia
Incidence of preeclampsia by race:
5.2% among black women
4% among Hispanics
3.9% among Native American women
3.8% among white women
3.5% among Asian women
Caughey, A., Stotland, N., Washington, A., Escobar, G., (2005)
Microsoft Office 2000
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Maternal and paternal ethnicity affects
preeclampsia rates :
Parents of differing ethnicity had an
increased rate of preeclampsia than those
with the same ethnicity(13%), with the
exception of Native Americans.
When parental ethnicity was the same
among Native Americans, the
rate of preeclampsia was
increased (9.7%)
Caughey et al., 2005
Microsoft Office 2000
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The parent who exerted the larger risk
of preeclampsia varied by ethnicity:
African-American maternal ethnicity
increased the risk of preeclampsia
Asian paternity was associated with the
lowest rate of preeclampsia
Microsoft Office 2000
Caughey et al., 2005
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Maternal race/ethnicity affects the
presentation and course of severe
preeclampsia.
Goodwin, A., Mercer, B. (2005)
Microsoft Office 2000
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African-American women were more likely to:
demonstrate severe and persistent hypertension
require intravenous antihypertensive therapy before
and after delivery
require chronic therapy after delivery and at 6-week
follow-up
Goodwin, A., Mercer, B., 2005
Microsoft Office 2000
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Caucasian women were more likely to:
present with less severe hypertension
demonstrate a higher incidence of HELLP
syndrome
develop thrombocytopenia and liver function
abnormalities
Goodwin, A., Mercer, B., 2005
Microsoft Office 2000
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In summary…
Insulin resistance
Hyperinsulinemia
Hypertriglyceridemia
Hypertriglyceridemia
Reduced HDL
Predominance of small, dense
LDL cholesterol
Reduced Placental
Perfusion
Abnormal vascular
remodeling of spiral
arteries
Stage 1
Maternal
Endothelial
Damage 
VASOSPASM
Release of toxic
factors
Stage 2
Maternal
Disease
Fetal
Effects
Increased
production of
free radicals and
lipid peroxides
+endothelial cell
damage
Inflammatory cytokines +
endothelial damage
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FETAL EFFECTS OF
PREECLAMPSIA
Putting together the pieces from a
fetal point of view
Fetal effects
We have looked at the two stage theory of the
pathophysiology of preeclampsia. As the maternal
disease progresses from its fetal beginnings, it will have
a clinical effect on the fetus.
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We will consider the following:
Fetal lipids
Genetics
Alterations in fetal growth (pop quiz!)
Hematologic implications (pop quiz!)
A fetal stress response
Microsoft Office 2000
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What is the effect on fetal lipids in a
preeclamptic pregnancy?
A 2004 study (Rodie, et al.) found these
alterations in lipid concentrations in the
cord blood of fetuses whose mothers had
preeclampsia:




Elevated total cholesterol
Elevated total cholesterol/HDL-C ratio
Elevated triglyceride levels
No correlation between maternal and fetal
lipid levels.
Rodie V.A., Caslake F.S., Sattar N., Ramsay J.E., Greer I.A.,
Greeman D.J., (2004)
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What is the relationship between fetal
lipids and maternal lipids in a
preeclamptic pregnancy?
Rodie, et al’s study found that fetal lipid levels
are not correlated to maternal lipid levels in
preeclampsia. Fetuses could have higher lipid
levels even in the presence of slightly elevated
maternal levels.
This implies that the circulating concentration of
maternal lipids available for placental uptake are
unlikely to determine fetal lipid concentration.
Rodie, et al. (2004)
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So what does this mean for the
fetus?
Placental transport of lipids in a preeclamptic
pregnancy may be adaptive or pathologic, but a
necessary fetal response to an adverse
intrauterine environment.

Transport mechanisms may be up-regulated to
compensate for oxidative stress and structural
damage to the placenta, so that these changes may
be a compensatory mechanism to supply the fetal
demands for an energy source.
Rodie, et al. (2004)
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Future impact for fetus
“Future impact from this study is unknown,
however other studies have demonstrated
that neonatal levels of Very Low Density
Lipoprotein (VLDL)-C (cholesterol), and
Low Density Lipoprotein (LDL)-C were
predictive of levels at age 13. These
lipoproteins are implicated in the
pathophysiology of atherosclerosis.”
Rodie, et al. (2004)
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Fetal Genetics and
Inheritance Patterns
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Inheritance patterns for a female
fetus in a preeclamptic pregnancy
Women born after a preeclamptic pregnancy have more
than twice the risk of having preeclampsia in their first
pregnancy.

This may be because their mothers pass on not only
independent genetic risk factors for the development of the
disease, but a genetic susceptibility as well.
The risk of developing preeclampsia during a second
pregnancy rather than a first, is diminished,
but these women still have twice the risk of
the general population of developing the
disease.
Microsoft Office 2000
Skjaerven R., Vatten L.J., Wilcox A.J., Ronning, T., Irgens L.M., Lie R.T. (2005)
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Siblings of women born to
preeclamptic mothers:
Sisters born as a result of pregnancies not affected by
preeclampsia are at lower risk, but they may also be
carrying their mother’s susceptibility genes. Thus, they
will also have twice the risk of developing the disease then
women with no family history of preeclampsia.
For brothers born as a result of a pregnancy not affected
by preeclampsia, their risk of fathering a preeclamptic
pregnancy was the same as men with no
family history of preeclampsia.
Skjaerven R., et al. (2005)
Microsoft Office 2000
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Inheritance patterns for a male
fetus in a preeclamptic pregnancy
Men born to preeclamptic mothers, moderately increase
the risk of preeclampsia in their partner’s first pregnancy.

This may be because these men received fetal genes capable of
triggering pre-eclampsia from their mothers, and pass these on
through their paternity. These fetuses then trigger the
development of the disease in their mothers.
Skjaerven, et al. (2005)
Microsoft Office 2000
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What are other clinical effects of
preeclampsia on the fetus?
Change in fetal growth patterns
What is the expected effect of preeclampsia on
intrauterine fetal growth? (click on answer
below)
A. Small for gestational age
B. Large for gestational age
C. No effect
Proceed to next question
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A. Small for Gestational Age
You are partially correct!


Research has demonstrated that SGA infants are
most commonly found in early onset
preeclampsia (maternal clinical signs manifested
before 37 weeks gestation).
Two theories exist:
 Iatrogenic prematurity (maternal status mandates
preterm delivery)
 Placental hypoperfusion related to impaired trophoblast
invasion impairs fetal growth.
Return to “last slide viewed” for more information 
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B. Large for Gestational Age
You are partially correct! How can this be?

Research has demonstrated that if the diagnosis of
preeclampsia is made after 37 weeks of gestation,
infants are of normal to LGA in size (especially in
gestations of > 40 weeks).
 There may be a subset of preeclampsia without placental
dysfunction. Or could fetal growth restriction be due to
other factors? Stay tuned for further research!
 Increase in maternal cardiac output late in pregnancy may
be a compensatory mechanism in the presence of
hypertension. The fetus can demand a greater share of
the maternal circulation for survival and gets it!
Return to “last slide viewed” for more information 
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C. No effect
Actually this is the only wrong answer!

Research has consistently demonstrated that
preeclampsia has an associated effect on
fetal growth.
Return to “last slide viewed” for more information 
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What other effects of preeclampsia
are found in the fetus?
Infants born to preeclamptic mothers
demonstrate neonatal thrombocytopenia.
(click on correct answer)
A. True
B. False
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A. True
Correct!

Proposed mechanism: One of the toxic factors
released by the hypoxic placenta in preeclampsia is
called sFlt1 (soluble fms-like tyrosine kinase). It acts
to deprive the endothelium of essential survival
factors contributing to endothelial dysfunction. It also
plays a role in mediating immune cell development in
the bone marrow and may contribute to the
pathogenesis of maternal preelampsia-induced
neonatal thrombocytopenia. Higher levels of sFlt1
have been found in cord blood of SGA babies of
preeclamptic mothers.
Tsao, P., Wei, S., Su, Y., Chou, H., Chen, S., Hsien, W. (2005)
Click here to proceed to next question
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B. False
Sorry, you are incorrect!

Return to question for more information
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Research has also indicated:
Elevated levels of ACE (angiotensinconverting enzyme) activity and ACE
mRNA have been found in umbilical
venous endothelial cells in preeclamptic
pregnancies in the presence of placental
hypoxia.
Critically thinking…..what implication does
this have?
Ito, M., Itakura, A., Ohno, Y., Nomura, M., Senga, T., Nagasaka, T., Mizutani, S.
(2002)
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Remember that ACE converts
angiotensin I to angiotensin II in the
renin-angiotensen-aldosterone
pathway…
The net effect is to increase blood
volume.
(for a brief review of this pathway, click on link below to use: Bowne, P.,
2004-2006, PATHO Interactive Physiology Tutorials. Then use the “back”
button on your browser to return to tutorial)
http://faculty.alverno.edu/bowneps/raa/raa%20end.htm
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So…
“The fetus needs the ability to redistribute
its blood flow during periods of hypoxia. In
response to hypoxic stress in
preeclampsia, if umbilical venous
endothelial cells produce ACE to stimulate
the conversion from angiotensin I to II,
then fetoplacental blood can be increased
and redistributed to vital organs.”
Ito, et. Al, (2002)
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FETAL MONITOR
STRIP REVIEW:
Putting it together
from an L&D
perspective
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Admitted into triage is:
JS, a 21 year old G1 P0 at 30 2/7 weeks, with c/o
headache x 3 days, unrelieved by Tylenol. She reports
“swelling” in her feet the past week that doesn’t go away
with elevation. She also admits to some intermittent
“blurry vision” x 3 days. Admitting VS :


BP 164/98, P 104, T 97.8, RR 24
VAS score for headache 8/10
Other significant findings are a fundal height of 26 cm,
and brisk patellar reflexes.
The following is her admission EFM strip:
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What is the FHR baseline?
1. 135 bpm
2. 130-140 bpm
3. 140-150 bpm
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Correct!
Remember, according to the new NICHD
Fetal Monitoring Terminology, that the
baseline is the mean FHR rounded to
increments of 5 beats per minute. So the
baseline will be expressed as a single
number.
Click here to proceed to next slide
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Try again!
Remember with the new NICHD Fetal
Heart Rate terminology that the FHR
baseline is no longer expressed as a
range.
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What is the FHR baseline variability?
1. Absent
2. Minimal
3. Moderate
4. Marked
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No,
The definition of absent variability is that
the amplitude range is undetectable.
Review the tracing again.
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No,
The definition of minimal variability is tha
the amplitude range is detectable, but 5
bpm or fewer. Review the tracing again.
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You are correct!
The definition of moderate (normal)
variability is an amplitude range of 6-25
bpm!
Click here to proceed to next slide
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No,
The definition of marked variability is an
amplitude range greater than 25 bpm.
Review the tracing again.
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Considering JS’s admission
assessment you are thinking…?
(click on answer below)
1. Headaches and visual changes are a common
c/o in pregnancy. JS has a normal presentation
for a patient at 30 2/7 weeks gestation.
2. The fetal monitoring strip is appropriate for
gestational age.
3. Considering JS’s BP, and report of symptoms,
she may be preeclamptic.
4. 2 and 3
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No….
There are some concerning pieces to the
puzzle. Use the “Last slide viewed” button,
below, to return to the question and try
again!
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You are partially correct…
The FHR tracing is appropriate for
gestational age:



Baseline is WNL
Variability is moderate.
Tracing is not considered reactive at this time.
Should it be? (click on an answer below)
 Yes
 No

But there is a better answer! Click here to
return to the question!
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At 30 2/7 weeks gestation,
the FHR tracing will not usually exhibit classic
“reactive” criteria-2 accelerations above the FHR
baseline of >15 bpm x > 15 sec in a 20 minute
period, due to the immaturity of the fetuses
central nervous system. Documented
accelerations of > 10 bpm x > 10 sec in a fetus <
32 weeks of gestation have been documented
as evidence of a healthy, well oxygenated
premature fetus.
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You are partially correct…
The concerning puzzle pieces are:




Elevated BP
Report of symptoms (headache, blurry vision, edema)
Fundal height of 26 cm (fundal height in cm should
correspond to weeks of gestation) may indicate an
SGA fetus.
Brisk patellar reflexes
But there is a more complete answer, click here
to return to the question.
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You are exactly right!
The concerning puzzle pieces are:




Elevated BP
Report of symptoms (headache, blurry vision, edema)
Fundal height of 26 cm (fundal height in cm should correspond
to weeks of gestation) may indicate an SGA fetus.
Brisk patellar reflexes
AND
The FHR tracing is appropriate for gestational age:


Baseline is WNL
Variability is moderate
Click here for next slide
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An hour later the tracing looks like this:
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JS’s assessment is unchanged from admission. Her BP is now
175/98, and a U/A sent on admission shows 3+ protein. Her
primary care giver decides to induce JS for a diagnosis of
preeclampsia. She is started on IV Magnesium Sulfate, and
Pitocin.
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What is concerning about the
previous tracing?
1. Nothing. It still appears appropriate for
gestational age.
2. Decreased FHR variability and a
questionable deceleration.
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No, you are not correct
Click here to review the tracing again
Microsoft Office 2000
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You are correct!
You have assessed JS’s monitor tracing
correctly!
What is the mechanism behind what you
are observing on the tracing?
1. Endothelial damage and vasospasm leading
to uteroplacental insufficiency.
2. Maternal hypertension
3. Placental edema
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Yes!
Congratulations! You have successfully
integrated theory and practice!
GOOD
JOB!
Microsoft Office 2000
Click here to continue
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No
Maternal hypertension is a symptom that
is also caused by this mechanism. Try
again!
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No
Try again!
Microsoft Office 2000
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Pitocin induction is started. Review
the next tracings as JS begins to
labor.
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JS’s BP is 210/95. What position should she be in?
1. Semi fowlers-that’s what she says is most comfortable to her
2. In the rocking chair to enhance her progress in labor
3. Side lying
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No
Not the best choice at this time! Try again!
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Correct!
Positioning JS in a side lying position
enhances cardiac return by removing the
weight of her uterus from compressing her
inferior vena cava. This in turn will
improve placental perfusion by enhancing
cardiac output. This position will also help
to lower JS’s BP.
To continue tracing review, click here
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Maternal BP=174/98
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What are these decelerations called? What are they indicative of?
1. Variable decelerations-cord compression
2. Early decelerations-fetal head compression
3. Late decelerations-uteroplacental insufficiency
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No
While their shape is similar to early
decelerations, the decelerations timing in
relation to the uterine contractions is
different. Click here to review the tracings
again.
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No
Think about the “whole picture” and the
fetal effects of the maternal disease
process. Are what you are seeing the
result of umbilical cord compression?
Remember that variable decelerations are
visually abrupt decreases in FHR, variable
in shape and in timing. Click here to
review the tracings again.
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Yes!
These are late decelerations. They have a
gradual decrease from the FHR baseline,
delayed in timing, with the nadir of the
deceleration occurring after the peak of the
contraction. The onset, nadir and recovery of
the deceleration occur after the onset, peak, and
ending of the contraction, respectively. Late
decelerations are indicative of uteroplacental
insufficiency, a result of endothelial damage and
vasospasm in the placental bed.
To continue with tracing review, click here
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Maternal BP=188/90
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As fetal intolerance to labor increases, as
evidenced by decreasing FHR variability and
late decelerations, JS is delivered by Cesarean
section.
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JS is delivered of a female infant
The baby weighs 1250 gms,demonstrating
evidence of growth restriction seen in early
onset preeclampsia.
Due to the baby’s prematurity and size,
she is admitted to the neonatal intensive
care unit.
This concludes the case study, click here to review the references
and acknowledgements.
Thank you!
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References
Bowne, P., 2004-2006. PATHO Interactive Physiology Tutorials. http://faculty.alverno.edu/bowneps/raa/raa%20end.htm
Braekke, K., Holthe, M.R., Harsem, N.K., Fagerhol, M.K., Staff, A. C. (2004). Calprotectin, a marker of inflammation, is elevated
in the maternal but not in the fetal circulation in preeclampsia. [Electronic version] American Journal of Obstetrics and
Gynecology, 193, 227-33.
Caughey, A., Stotland, N., Washington, A., Escobar, G. (2005). Maternal Ethnicity, Paternal Ethnicity, and Paternal Ethnic
Discordance: Predictors of Preeclampsia. [Electronic version] Obstetrics & Gynecology, 106(1), 156-161.
Chappell, L.C., Seed, P.T., Briley, A.B., Kelly, F.J., Hunt, B.,J., Charnock-Jones, S., Mallet, A.I., Poston, L. (2002). A longitudinal
study of biochemical variables in women at risk of preeclampsia. [Electronic version] American Journal of Obstetrics and
Gynecology, 187(1), 127-136.
Goodwin, A., Mercer, B. (2005). Does maternal race or ethnicity affect the expression of severe preeclampsia? [Electronic
version] Americal Journal of Obstetrics and Gynecology, 193(3), 973-978.
Gratacos, E. (2000). Lipid-mediated endothelial dysfunction: a common factor to preeclampsia and chronic vascular disease.
[Electronic version] European Journal of Obstetrics & Gynecology and Reproductive Biology, 92: 63-66.
Innes, K.E., Weitzel, L., Laudenslager, M. (2005). Altered Metabolic Profiles among Older Mothers with a History of
Preeclampsia. [Electronic version] Gynecologic and Obstetric Investigation, 59: 192-201.
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References
Ito, M., Itakura, A., Ohno, Y., Nomura, M., Senga, T., Nagasaka, T., Mizutani, S. (2002) Possible Activation of the ReninAngiotensin System in the Feto-Placental Unit in Preeclampsia. [Electronic version] The Journal of Clinical Endocrinology &
Metabolism, 87(4):1871-1878.
Khan, F., Belch, J.J.F., MacLeod, M., Mires, G. (2005). Changes in Endothelial Function Precede the Clinical disease in Women
in Whom Preeclampsia Develops. [Electronic version] Hypertension, 46: 1123-1128.
Lindheimer, M.D., (2005). Unraveling the mysteries of preeclampsia. [Electronic version] American Journal of Obstetrics and
Gynecology, 193: 3-4.
Myers, PZ (2005) Mechanisms of preeclampsia. Retrieved from
http://pharyngula.org/index/weblog/comments/mechanisms_of_preeclampsia/
National Institute of Health National High Blood Pressure Education Program Working Group on High Blood Pressure in
Pregnancy (NIH publication No. 00-3029, July 2000).
Odegard, R.A., Vatten, L.J., Nilsen, S.T., Salvesen, K.A., Austgulen, R. (2000) Preeclampsia and Fetal Growth. [Electronic
version] Obstetrics and Gynecology, 96(6): 950-955.
Polin, R.A., Fox, W.W. (2004). Fetal and Neonatal Physiology (3rd ed.), Chapter 16, Maternal Cardiovascular Disease and Fetal
Growth and Development. Philadelphia, P.A., Saunders, pp 147-155.
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References
Porth, Carol Mattson (2005 ) Pathophysiology-Concepts of Altered Health States (7th ed.), Philadelphia, P.A., Lippincott.
Rasmussen, S., Irgens, L.M. (2003) Fetal Growth and Body Proportion in Preeclampsia. [Electronic version] Obstetrics and
Gynecology, 101(3): 575-583.
Redman C.W., Sargent I.L. (2005). Latest Advances in Understanding Preeclampsia. [Electronic version] Science, 308:15921594.
Roberts J.M, Gammill H.S. (2005). Preeclampsia: Recent Insights. [Electronic version] Hypertension, 46: 1243-1249.
Rodie V.A., Caslake M.J,. Stewart F., Sattar N., Ramsay J.E., Greer I.A., Freeman D.J. (2004). Fetal cord plasma lipoprotein
status in uncomplicated human pregnancies and in pregnancies complicated by pre-eclampsia and intrauterine growth
restriction. Atherosclerosis, 176: 181-187.
Skjaerven R., Vatten L.J., Wilcox A.J., Ronning, T., Irgens L.M., Lie R.T. (2005) Recurrence of preeclampsia across
generations: exploring fetal and maternal genetic components in a population based cohort. [Electronic version] BMJ,
doi:10.1136/bmj. 38555.462685.8F.
STAT!Ref Online Dictionary. Accessed through http://www.mcw.edu/display/router.asp?docid=10306
Tsao, P., Wei, S., Su, Y., Chou, H., Chen, C., Hsieh, W. (2005) Excess Soluble fms-Like Tyrosine Kinase 1 and Low Platelet
Counts in Premature Neonates of Preeclamptic Mothers. Pediatrics, 116(2): 468-472.
Van Pampus, M.G., Aarnoudse, J.G. (2005). Long-Term Outcomes After Preeclampsia. [Electronic version] Clinical
Obstetrics and Gynecology, 48(2), 489-494.
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References
Wagner, L.K. (2004). Diagnosis and Management of Preeclampsia. [Electronic version] American Family Physician, 70(12),
2317-2324.
Warden M., Euerle B. (2005). Preeclampsia (Toxemia of Pregnancy) Retrieved from
http://www.emedicine.com/med/topic1905.htm
Xiong, X., Mayes, D., Demianczuk, N., Olson, D.M., Davidge, S.T., Newburn-Cook, C., Saunders, L.D. (1999) Impact of
pregnancy-induced hypertension on fetal growth. [electronic version] American Journal of Obstetrics and Gynecology, 180(1),
207-213.
Zhong X.Y., Gebhardt S., Hillerman R., Tofa K.C., Holzgreve W., Hahn S. (2005) Parallel Assessmant of Circulatory Fetal DNA
and Cortidotropin-Releasing Hormone mRNA I Early- and Late-Onset Preeclampsia. [Electronic version] Clinical Chemistry,
51(9),1730-1733.
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Acknowledgements
Julie Bohlen, Senior Vice President of eMedicine, for permission to link to
eMedicine’s website for further information (Permission granted via email 4/26/06).
Professor Patricia Bowne, Alverno College, for her generous permission to use her
published tutorials as resources.
Professor Christopher Redman, Nuffield Department of Obstetrics and Gynaecology
at John Radcliffe Hospital, Oxford, England, for his permission to use the illustrations
of normal and abnormal placentation in preeclampsia (Permission obtained via email
2/14/06).
James M. Roberts, MD, Magee-Womens Research Institute, for his permission to use
the graphic representation of the two stage model of preeclampsia (Permission
obtained via email 3/10/06).
To contact the authors:
Nancy Rogers RNC BSN nrogers@fmlh.edu
Leslie Dittus-Yaeger RNC BSN ldittus@fmlh.edu
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The end
THANK YOU!
Microsoft Office 2000
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