Preeclampsia and Peripartum Cardiomyopathy
BRIEF REPORTS
in a 24-Year-Old Woman
Katie Fellner, MS1; Shawn Skarpnes, MD2
1
Louisiana State University Health Sciences Center School of Medicine, New Orleans, LA
2
Department of Family Medicine, Baton Rouge General Hospital, Baton Rouge, LA
ABSTRACT
Herein we report the case of a 24-year-old wom-
an who presented with gestational hypertension
and a history of preeclampsia with a previous
pregnancy as well as a family history of
preeclampsia and eclampsia. She subsequently
developed a definitive preeclampsia with pro-
teinuria in the 30th week of gestation, which ne-
cessitated a caesarian delivery. Two weeks post-
partum the patient developed dyspnea with bi-
lateral pulmonary infiltration and was hospital-
ized for an atypical pneumonia. After comple-
tion of an antibiotic course she continued to ex-
perience dyspnea and orthopnea and ultimately
developed systolic heart failure with an ejection
fraction of 30%. Following treatment with di-
uresis and rate control, she greatly improved.
This case demonstrates the importance of close
monitoring of patients with atypical preeclamp-
sia by a primary care and coordinated specialties
team. It demonstrates a sequential progression
of worsening hypertension, preeclampsia, and
Corresponding Author: Katie Fellner, MS, LSU Health Sciences
Center School of Medicine, 533 Bolivar St # 511, New Orleans,
LA 70112.
Email: sfell1@lsuhsc.edu
The authors claim no conflicts of interest or disclosures.
AMSRJ 2015; 2(1):103-111
http://dx.doi.org/10.15422/amsrj.2015.05.015
AMSRJ 2015 Volume 2, Number 1
peripartum cardiomyopathy driven by the un-
derlying mechanism of elevated systemic vas-
cular resistance. It also proposes an association
of peripartum cardiomyopathy with increased
gestational body mass index (BMI).
INTRODUCTION
Preeclampsia affects 4.6 percent (95% confi-
dence interval [CI] 2.7-8.2) of pregnancies
worldwide.1 The criteria for the diagnosis of
preeclampsia include an elevated blood pressure
occurring after 20 weeks of gestation and pro-
teinuria (≥0.3 g of protein in a 24-hour urine
sample, a protein (mg/dL):creatinine (mg/dL)
ratio of ≥ 0.3 or a 1+ dipstick).2 In patients with
new onset hypertension, signs of end organ dam-
age may be substituted for proteinuria to make
the diagnosis of preeclampsia. In most cases
symptoms develop before 34 weeks of gesta-
tion. Early-onset preeclampsia occurs in 10% of
patients and is associated with an increased mor-
bidity to the mother and fetus, increasing the risk
of fetal death greater than five-fold and increas-
ing the risk of perinatal death/severe neonatal
morbidity sixteen-fold.3,4 Our patient presented
with atypical signs of preeclampsia at 25 weeks
of gestation but did not meet definitive criteria
105
 PREECLAMPSIA AND PERIPARTUM CARDIOMYOPATHY
until 30 weeks of gestation, at which point deliv-
ery was induced due to the development of pla-
cental insufficiency and intrauterine growth re-
BRIEF REPORTS
striction. Preeclampsia presentation is highly
variable and a high index of suspicion for devel-
opment during the third trimester must be main-
tained, especially in the setting of multiple risk
factors as was the case for our patient.5
Preeclampsia may lead to eclampsia, the devel-
opment of tonic-clonic seizures and coma dur-
ing delivery that can result in fetal and/or mater-
nal demise. Peripartum cardiomyopathy is a
form of systolic heart failure which affects
1/1300-4000 live births.6 Cardiomyopathy can
develop in a small subset of preeclampsia cases;
it is important to consider this etiology in the
setting of pulmonary infiltration consistent with
transudative versus exudative fluid.7 If untreat-
ed, peripartum cardiomyopathy can lead to atrial
or ventricular arrhythmia, thromboembolism, or
sudden cardiac death. An involved and mindful
primary care and coordinated specialties team is
essential to the successful case management of
the preeclamptic patient.
CASE PRESENTATION
A 24-year-old African American woman first
presented at 19 weeks gestation to clinic after an
emergency department (ED) visit for abdominal
pain and a blood pressure of 190/90 mmHg (Ta-
ble 1). Upon initial presentation she was nor-
motensive and not experiencing pain. The pa-
tient had a positive family history of preeclamp-
sia and eclampsia; her mother had an eclamptic
episode and miscarriage of twins within a span
of five normal pregnancies. The patient’s first
pregnancy was complicated by preeclampsia,
requiring induction at 36 weeks of gestation.
The patient continued to return for prenatal vis-
its and at 28 weeks presented with elevated
106 AMSRJ 2015 Volume 2, Number 1
home blood pressures, 6/10 migraine with bilat-
eral visual scotomas, unremitting abdominal
pain, 2+ pitting pedal edema, 1+ facial and hand
edema, and trace urine protein. The patient’s
weight had continued to increase, now measur-
ing 219 pounds as compared to a pre-pregnancy
weight of 180 pounds. She was noted to have
gained 12 pounds within the last 2 weeks. Fundal
height was 26 cm and fetal heart tones were in
the range of 140 beats per minute. At that time
the patient was started on labetalol 100 mg and
referred to a perinatologist.
An ultrasound conducted at 29 weeks revealed a
single fetus in a vertex position with an estimat-
ed weight of 2 pounds, 9 ounces (less than 5% of
normal fetal growth). As previous scans had re-
vealed the fetus to be at the 25th percentile for
growth, intrauterine growth restriction became a
primary concern. The ultrasound also revealed a
posterior, premature grade III placenta with ex-
tensive basal calcifications and a chorionic plate
interrupted by indentations, a finding which
could lead to placental insufficiency. The pa-
tient was admitted at that time for preeclamptic
evaluation and received a course of beclometha-
sone to expedite fetal lung maturity in anticipa-
tion of premature delivery. Labetolol was in-
creased to 200 mg.
At 30 6/7 weeks of gestation, the patient present-
ed to the ED with headache, scotomata, and
blurred vision. She was found to have a blood
pressure of 160/110 mmHg and 2+ proteinuria.
Perinatology noted that her amniotic fluid vol-
ume was decreased markedly, with an amniotic
fluid index (AFI) of 6.5 cm as compared to
7.9cm-27.3 cm from 15-40 weeks gestation.8 At
this time it was noted the patient was experienc-
ing irregular contractions. Pelvic examination
confirmed cervical dilation of 1-2 cm. After in-
creasing labetolol to 300 mg, the amniotic fluid
volume improved to an AFI of 9 cm. However
the fetal biophysical profile score was 6, with no
evidence of fetal breathing, including in re-
 PREECLAMPSIA AND PERIPARTUM CARDIOMYOPATHY

Weeks%Gestational%Age%(WGA) Pre3pregnancy 19%WGA 20%WGA 25%WGA 27%WGA 28%WGA 29%WGA 30%WGA 7%days%post3partum 10%days%post3partum 30%days%post3partum
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Weight%(pounds) 180 204.8 207.2 219 219 219 219 201.4 202.9 200.86
Vital%Signs %% %%%%%%%BMI 32.9 37.5 37.9 40.1 40.1 40.1 40.1 36.8 37.1 36.8
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Blood%Pressure%(mm%Hg) 190/90 126/84 118/83 132/89 162/93 129/83 160/110 165/130 163/111 122/78
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Hear%Rate%(beats/minute) 109 97 83 110 94 124 127 98

BRIEF REPORTS
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Respiratory%Rate%(breaths/minute) 18 22 20 18 18 18 23 18
Fetal %% %%%%%%%%%%%%%%%%%%%Fundal%Height%(cm) 18 18 25 26 26 28 28
Monitoring%%%%%%Fetal%heart%tones%(beats/minute) 140 150 150 140 140 140 140
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Urine%Protein trace trace negative negative trace trace 2+ Trace
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Serum%Creatinine 0.4 0.6 0.5 0.5 0.5 0.6 0.7 0.8
%Lab%Results%%%%%Platelets%(per%mm^3) 278 288 268 288 268 480 437 384
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Alanine%Aminotransferase%(IU/L) 17 15 12 40 26 30 18
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Aspartate%Aminotransferase%(IU/L) 34 16 18 31 16 25 15
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Brain%natriuretic%peptide%(pg/mL) 268.1 397
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%E/A%Ratio 1.2 1.5
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Pulmonary%Arterial%Pressure%(mmHg) 25 30 40
Imaging %%%%%%%%%%%%%%%Mitral%E3F%slope%(mm/s) 70 217 100
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Left%Ventricular%Ejection%Fraction%(%) 70 60 30
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%LV%wall%thickness%(cm) 1.2 1.1 1.1
headache,;mild; 6/10;migraine,; headache,; orthopnea,;dyspnea,; dypsnea 4;pillow;orthopnea,;2+;
pedal;edema scotomata,;2+; scotomata,; crackles lower;extremity;edema,;
pitting;pedal; blurred; dypsnea;on;exertion;after;
Clinical%Signs edema,;1+;facial; vision walking;50;feet,;jugular;
and;hand;edema; venous;distension,;
bilateral;basilar;crackles,;
S3;gallop
labetolol;100;mg,; labetolol;200;mg,; labetolol; amoxicillin/clavulani furosemide;40mg,;
Perinatology; beclomethasone;12.5; 300;mg c;acis;875;mg;for;10; lisinopril;5;mg,;metoprolol;
referral mg;IM;Q12,;amoxicillin; days,;naproxen;500; 25;mg,;albuterol;90;mcg;as;
Treatment for;10;days; mg;every;8;hours needed

Table 1. Vital Signs, Fetal Monitoring, Laboratory Results, Imaging, Clinical Signs, and Treatment in Pre- to Postpartum Period !

sponse to fetal acoustic stimulation. The umbili- Based on clinical signs and radiology, peripar-
cal artery resistance was also found to be elevat- tum cardiomyopathy was a concern and the pa-
ed with a systolic/diastolic blood flow ratio of tient was sent to the cardiology outpatient clinic
3.66 (greater than 3 at ≥28 weeks of gestation for echocardiography. The patient, however, did
predicts a high risk of adverse outcome).9 Fetal not present to the cardiology clinic for follow-
heart rate remained stable; however, the patient up.
was induced to deliver given the heightened
concern for complications. During induction Three days later, the patient presented to the ED
with oxytocin, late decelerations of fetal heart with a complaint of dyspnea, subjective fever,
rate were noted, and an emergency C-section and chills. She was found to have an uncompen-
was warranted. A male infant weighing 1260 g
(2.77 pounds) was safely delivered. He had an
Apgar score of 8 with healthy respiration and
circulation. The patient was seen by her family
practitioner 7 days post-partum for inspection of
the incision site. The patient also complained of
shortness of breath and right chest pain. Upon
auscultation the patient was found to have crack-
les in the right middle lobe base, orthopnea, and
continued expectoration of a clear, milky white
fluid from her lungs. A chest radiograph demon-
strated a consolidation in the right middle lobe
suspicious for pneumonia versus pulmonary
edema. The cardiac silhouette demonstrated a
heart that had enlarged to greater than half of the Figure 1. Chest radiograph demonstrating right middle lower
width of the thorax at its widest point (Figure 1). lobe pulmonary infiltration and concurrent cardiomyopathy.

AMSRJ 2015 Volume 2, Number 1 107

 PREECLAMPSIA AND PERIPARTUM CARDIOMYOPATHY
sated respiratory alkalosis with a pH of 7.5,
pCO2 of 24, bicarbonate of 18, pO2 of 67 and a
hemoglobin saturation of 92.7. She also had an
BRIEF REPORTS
extremely elevated d-dimer of 2.21 µg/mL (nor-
mal values= <0.5 µg/mL), an increased platelet
count of 480/mm3, an elevated troponin of 0.05
ng/mL, and a slightly elevated chloride of 110
mEq/L. Uric acid was also elevated at 7.7 mEq/
L, which could indicate renal dysfunction due to
systemic shock. The patient continued to have a
decreased O2 saturation on exertion.
Sputum gram stain showed elevated polymor-
phonuclear cells and moderate respiratory flora
while chest radiography continued to display the
right middle lobe consolidation. The patient was
treated with amoxicillin/clavulanic acid and
naproxen; she continued to improve while hos-
pitalized. The patient’s respiratory symptoms
resolved with treatment of the atypical pneumo-
nia, and she was discharged three days later.
Echocardiogram at this time found trace tricus-
pid regurgitation and trace pulmonary insuffi-
ciency with a pulmonary arterial pressure of 30
mmHg. The mitral valve E-F slope was 217 mm/
sec and the D-E separation was 22 mm indicat-
ing a mild to moderate mitral valve regurgitation
with an E/A ratio of 1.5. The left atrium was
found to be enlarged at 4.2 cm (normal range
1.9-3.8 cm). Left ventricular ejection fraction at
this time, however, was preserved at 60%.
Thirteen days later the patient presented to her
primary care practitioner for follow-up of the
pneumonia. After completing the antibiotic
course, the patient continued to experience dys-
pnea and cough exacerbated by the supine posi-
tion. She reported expectorating a clear fluid
from the lungs and was tachypneic. She was then
referred to a pulmonologist to follow-up for
pneumonia and investigate alternative causes of
the dyspnea.
Eight days later the patient presented to the pul-
monology clinic. At that time she reported sig-
108 AMSRJ 2015 Volume 2, Number 1
nificant dyspnea on exertion after walking less
than 50 feet as well as significant paroxysmal
nocturnal dyspnea with 4-pillow orthopnea. She
had a cough productive of white sputum but no
complaint of fever or chills. Upon physical exam
she had apparent jugular venous distension and
bilateral basilar crackles but did not have wheez-
ing or rhonchi. Cardiovascular exam revealed an
S3 gallop and 2+ lower extremity edema. A
chest radiograph showed a mildly enlarged car-
diovascular silhouette with diffuse bilateral
airspace opacities. The patient was admitted to
the hospital, referred to a cardiologist, and was
started on furosemide 40mg.
The echocardiogram completed the next day
demonstrated mild tricuspid regurgitation, trace
pulmonary insufficiency with a pulmonary arte-
rial pressure of 40 mmHg, and moderate mitral
regurgitation with an ejection fraction of 30%.
At that time she was diagnosed with systolic
heart failure exacerbation of peripartum car-
diomyopathy and started on a beta blocker.
DISCUSSION
Preeclampsia results in uteroplacental hypoxia,
an imbalance in angiogenic and anti-angiogenic
proteins, oxidative stress, maternal endothelial
dysfunction, and elevated systemic inflamma-
tion (Figure 2).10,11 It is accompanied by in-
creased sensitivity of the maternal vasculature to
pressor agents leading to vasospasm and hypop-
erfusion of multiple organs. Microthrombi de-
velop from the activation of the coagulation cas-
cade. Vasodilation results in plasma leakage,
causing edema. The pathogenesis is thought to
arise from placental insufficiency secondary to
failure of the trophoblast to invade the my-
ometrium. There is decreased placental secre-
tion of the vasodilatory and growth factors
adrenomedulin, prostacyclins, thromboxane
 PREECLAMPSIA AND PERIPARTUM CARDIOMYOPATHY
Figure 2. Hypertrophic decidual vasculopathy and infarction of spiral
placental arteries in preeclamptic placental tissue.12 Hematoxylin &
eosin (H&E) stain, 100x magnification.
A2, and vascular endothelial growth factor
(VEGF). The expression of the angiotensin I re-
ceptor is increased, resulting in a decrease in
nitric oxide and increase in endothelin-1, caus-
ing an increase in maternal systemic vascular
resistance in an attempt to improve placental
perfusion.3 Inflammatory mediators such as tu-
mor necrosis factor-alpha and interleukin-6 are
also secreted which drive maternal hyperten-
sion, endothelial dysfunction, and oxidative
stress. Cerebral edema and hypertension can re-
sult in the seizures and coma of eclampsia.
Our patient did not meet the definitive criteria
for the diagnosis of preeclampsia before 30
weeks of gestation. She had elevated blood pres-
sures which elicited clinical signs of hyperten-
sion such as headache, scotomata, and pul-
monary edema, which are considered signs of
severe preeclampsia beginning at week 25.9 She
presented with worsening hypertension
throughout gestation superimposed upon a
background of chronic hypertension but did not
present with signs of end organ damage such as
platelet count <100,000/uL, serum creatinine
>1.1 mg/dL, or liver transaminases twice the
normal concentration. She did have certain risk
factors for preeclampsia, such as preeclampsia
AMSRJ 2015 Volume 2, Number 1
with her first pregnancy (increases the risk 7-
fold; relative risk 7.19, 95% CI 5.85-8.83), fami-
ly history of preeclampsia (mother with history
BRIEF REPORTS
of eclampsia), blood pressure >130/80 mmHg at
the first prenatal visit, BMI >26, and black
race.13 Our patient presented with an atypical
preeclampsia, with early clinical signs in the ab-
sence of diagnostic criteria and then rapid devel-
opment of a definitive early-onset preeclampsia
at 30 weeks gestation, which has a particularly
bad prognosis.3 This development highlights the
importance of close monitoring in patients with
preeclampsia risk factors which may not present
with the classic criteria for preeclampsia diagno-
sis.
Systolic heart failure can result from decompen-
sation of a dilated left ventricle which had previ-
ously maintained normal ejection fraction by in-
creasing left ventricular end diastolic pressure
and end diastolic volume. The elevated systemic
vascular resistance becomes an afterload that the
left ventricle can no longer approximate, and
eventually the ejection fraction can no longer be
maintained. Mitral valve regurgitation results
due to chamber dilation, and an early diastolic
filling S3 may be heard. The elevation of sys-
temic vascular resistance that occurs in
preeclampsia can contribute to the development
of peripartum cardiomyopathy. As the pressure
in the left ventricle increases, it is transmitted to
the pulmonary veins and lungs, resulting in fluid
transudation into the alveolar spaces and pul-
monary edema. Alveolar macrophages that en-
gulf transudated erythrocytes and proteins are
termed “heart failure cells” (Figure 3).14 The
phenomenon of excess pulmonary arterial pres-
sure elicits pulmonary edema, particularly in the
postpartum period in the preeclamptic patient.
Our patient did develop an elevated pulmonary
arterial pressure of 40 mmHg at thirty days post-
partum, which contributed to the systolic heart
failure.15 In addition to this mechanism, there is
evidence that other factors play a role. Systolic
strain was found to be depressed in preeclamptic
109
 PREECLAMPSIA AND PERIPARTUM CARDIOMYOPATHY
BRIEF REPORTS
Figure 3. Hemosiderin-laden heart failure cells in bronchoalveolar
lavage fluid.15 H&E stain, 40x magnification.
patients compared to pregnant women with non-
proteinuric hypertension with similar resting
blood pressure.16
It is important to consider the etiology of peri-
partum cardiomyopathy in patients presenting
with pneumonia-like vs. transudative symp-
toms. Our patient was treated ten days post-par-
tum for pneumonia with only normal respiratory
flora cultured. It was atypical, possibly caused
by an imbalance of normal flora within the pul-
monary interstitium and a nidus for infection
created by the presence of excess basilar fluid.
The patient’s dyspnea did not resolve upon com-
pletion of an antibiotic course. At that time, mild
cardiomegaly was noted on chest x-ray and a
cardiogenic pulmonary edema was investigated.
Thirty days post-partum the patient was noted to
have clinical signs of heart failure. A diuretic
was started and the patient’s clinical features im-
proved markedly. She then developed moderate
mitral regurgitation, mild tricuspid regurgita-
tion, pulmonic insufficiency, and an ejection
fraction of 30%. The ejection fraction during
and after pregnancy had previously been pre-
served at or above 53%. The patient’s brain na-
triuretic peptide (BNP) was elevated to 397 pg/
mL at 31 days post-partum, supporting the diag-
nosis of systolic heart failure.
The patient’s development of systolic heart fail-
ure in conjunction with preeclampsia through-
out the pregnancy was unexpected but promptly
treated with rapid amelioration of symptoms.
110
This fortunate outcome highlights the impor-
tance of close monitoring and integrated conti-
nuity of care among the primary care and spe-
cialty consulting physicians of the treatment
team. Awareness of potential risks and compli-
cations can allow for rapid diagnosis and prompt
treatment. Prophylaxis against seizures during
delivery is of the utmost importance and would
have prevented morbidity to the mother and fe-
tus in less closely monitored situations.
Obesity and an elevated BMI are associated with
an increased risk for preeclampsia.17 Prenatal
counseling for lower calorie diets and moderate
exercise before and during pregnancy may help
decrease the severe risks of gestational hyper-
tension and preeclampsia to mother and fetus.
The importance of awareness among physicians
of the risks of these clinical features in healthy-
appearing gravid young women, as well as con-
tinuity among primary and specialty care
providers is the key to a safe pregnancy for wom-
en with preeclampsia.
LEARNING POINTS
• Acute on chronic hypertension in pregnant
women should be closely monitored due to
the potential late-term development of
preeclampsia.
• Development of peripartum cardiomyopa-
thy, which can present with respiratory dis-
tress, is a risk associated with preeclampsia.
• Preeclampsia is associated with intrauter-
ine growth retardation that may necessitate
preterm delivery and intrapartum seizure
prophylaxis.
AMSRJ 2015 Volume 2, Number 1
 PREECLAMPSIA AND PERIPARTUM CARDIOMYOPATHY
ACKNOWLEDGEMENTS
The authors would like to acknowledge the as-
sistance of Dr. Brian Schulte, Dr. Duane Neu-
mann, Dr. Stephen Brierre, Dr. Lance Lamotte,
Dr. Wayne Gravois, Dr. Vincent Shaw, Dr. Bri-
an Benson, and Dr. Kevin Reed in the treatment
of this patient and provision of documents.
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