Download Preeclampsia and Peripartum Cardiomyopathy in a 24-Year

BRIEF REPORTS
Preeclampsia and Peripartum Cardiomyopathy
in a 24-Year-Old Woman
Katie Fellner, MS1; Shawn Skarpnes, MD2
Louisiana State University Health Sciences Center School of Medicine, New Orleans, LA
2
Department of Family Medicine, Baton Rouge General Hospital, Baton Rouge, LA
1
ABSTRACT
Herein we report the case of a 24-year-old woman 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 proteinuria in the 30th week of gestation, which necessitated a caesarian delivery. Two weeks postpartum the patient developed dyspnea with bilateral pulmonary infiltration and was hospitalized for an atypical pneumonia. After completion of an antibiotic course she continued to experience dyspnea and orthopnea and ultimately
developed systolic heart failure with an ejection
fraction of 30%. Following treatment with diuresis and rate control, she greatly improved.
This case demonstrates the importance of close
monitoring of patients with atypical preeclampsia 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: [email protected]
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
peripartum cardiomyopathy driven by the underlying mechanism of elevated systemic vascular resistance. It also proposes an association
of peripartum cardiomyopathy with increased
gestational body mass index (BMI).
INTRODUCTION
Preeclampsia affects 4.6 percent (95% confidence 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 proteinuria (≥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 damage may be substituted for proteinuria to make
the diagnosis of preeclampsia. In most cases
symptoms develop before 34 weeks of gestation. Early-onset preeclampsia occurs in 10% of
patients and is associated with an increased morbidity to the mother and fetus, increasing the risk
of fetal death greater than five-fold and increasing 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
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BRIEF REPORTS
until 30 weeks of gestation, at which point delivery was induced due to the development of placental insufficiency and intrauterine growth restriction. Preeclampsia presentation is highly
variable and a high index of suspicion for development during the third trimester must be maintained, especially in the setting of multiple risk
factors as was the case for our patient.5
Preeclampsia may lead to eclampsia, the development of tonic-clonic seizures and coma during delivery that can result in fetal and/or maternal 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 untreated, 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 (Table 1). Upon initial presentation she was normotensive and not experiencing pain. The patient had a positive family history of preeclampsia 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 visits and at 28 weeks presented with elevated
106
home blood pressures, 6/10 migraine with bilateral 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 measuring 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 estimated weight of 2 pounds, 9 ounces (less than 5% of
normal fetal growth). As previous scans had revealed 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 extensive basal calcifications and a chorionic plate
interrupted by indentations, a finding which
could lead to placental insufficiency. The patient was admitted at that time for preeclamptic
evaluation and received a course of beclomethasone to expedite fetal lung maturity in anticipation of premature delivery. Labetolol was increased to 200 mg.
At 30 6/7 weeks of gestation, the patient presented 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 volume 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 experiencing irregular contractions. Pelvic examination
confirmed cervical dilation of 1-2 cm. After increasing 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-
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Weeks%Gestational%Age%(WGA)
Pre3pregnancy 19%WGA 20%WGA 25%WGA
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Weight%(pounds)
Vital%Signs %% %%%%%%%BMI
27%WGA 28%WGA
29%WGA
30%WGA
7%days%post3partum
10%days%post3partum 30%days%post3partum
204.8
207.2
219
219
219
219
201.4
202.9
32.9
37.5
37.9
40.1
40.1
40.1
40.1
36.8
37.1
36.8
126/84
118/83
132/89
162/93
129/83
160/110
165/130
163/111
122/78
109
97
83
110
94
124
127
98
18
22
20
18
18
18
23
18
18
25
26
28
28
150
140
140
140
140
negative negative
trace
trace
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Blood%Pressure%(mm%Hg)
190/90
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Hear%Rate%(beats/minute)
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Respiratory%Rate%(breaths/minute)
Fetal %% %%%%%%%%%%%%%%%%%%%Fundal%Height%(cm)
Monitoring%%%%%%Fetal%heart%tones%(beats/minute)
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Urine%Protein
18
140
150
trace
trace
26
2+
200.86
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
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Aspartate%Aminotransferase%(IU/L)
34
16
18
31
16
25
18
15
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Brain%natriuretic%peptide%(pg/mL)
268.1
397
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%E/A%Ratio
1.2
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Pulmonary%Arterial%Pressure%(mmHg)
25
30
40
Imaging %%%%%%%%%%%%%%%Mitral%E3F%slope%(mm/s)
70
217
100
1.5
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%Left%Ventricular%Ejection%Fraction%(%)
70
60
30
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%LV%wall%thickness%(cm)
1.2
1.1
1.1
headache,;mild;
pedal;edema
Clinical%Signs
Treatment
6/10;migraine,;
scotomata,;2+;
pitting;pedal;
edema,;1+;facial;
and;hand;edema;
headache,; orthopnea,;dyspnea,;
scotomata,; crackles
blurred;
vision
labetolol;100;mg,; labetolol;200;mg,;
labetolol;
Perinatology;
beclomethasone;12.5; 300;mg
referral
mg;IM;Q12,;amoxicillin;
for;10;days;
dypsnea
4;pillow;orthopnea,;2+;
lower;extremity;edema,;
dypsnea;on;exertion;after;
walking;50;feet,;jugular;
venous;distension,;
bilateral;basilar;crackles,;
S3;gallop
amoxicillin/clavulani furosemide;40mg,;
c;acis;875;mg;for;10; lisinopril;5;mg,;metoprolol;
days,;naproxen;500; 25;mg,;albuterol;90;mcg;as;
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 umbilical artery resistance was also found to be elevated with a systolic/diastolic blood flow ratio of
3.66 (greater than 3 at ≥28 weeks of gestation
predicts a high risk of adverse outcome).9 Fetal
heart rate remained stable; however, the patient
was induced to deliver given the heightened
concern for complications. During induction
with oxytocin, late decelerations of fetal heart
rate were noted, and an emergency C-section
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 crackles in the right middle lobe base, orthopnea, and
continued expectoration of a clear, milky white
fluid from her lungs. A chest radiograph demonstrated 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
width of the thorax at its widest point (Figure 1).
BRIEF REPORTS
180
!
Based on clinical signs and radiology, peripartum cardiomyopathy was a concern and the patient was sent to the cardiology outpatient clinic
for echocardiography. The patient, however, did
not present to the cardiology clinic for followup.
Three days later, the patient presented to the ED
with a complaint of dyspnea, subjective fever,
and chills. She was found to have an uncompen-
Figure 1. Chest radiograph demonstrating right middle lower
lobe pulmonary infiltration and concurrent cardiomyopathy.
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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
extremely elevated d-dimer of 2.21 µg/mL (normal 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 polymorphonuclear 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 hospitalized. The patient’s respiratory symptoms
resolved with treatment of the atypical pneumonia, and she was discharged three days later.
Echocardiogram at this time found trace tricuspid regurgitation and trace pulmonary insufficiency 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 indicating 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 dyspnea and cough exacerbated by the supine position. 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 pulmonology clinic. At that time she reported sig-
108
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 wheezing or rhonchi. Cardiovascular exam revealed an
S3 gallop and 2+ lower extremity edema. A
chest radiograph showed a mildly enlarged cardiovascular 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 arterial 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 cardiomyopathy 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 inflammation (Figure 2).10,11 It is accompanied by increased sensitivity of the maternal vasculature to
pressor agents leading to vasospasm and hypoperfusion of multiple organs. Microthrombi develop from the activation of the coagulation cascade. 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 myometrium. There is decreased placental secretion of the vasodilatory and growth factors
adrenomedulin, prostacyclins, thromboxane
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A2, and vascular endothelial growth factor
(VEGF). The expression of the angiotensin I receptor is increased, resulting in a decrease in
nitric oxide and increase in endothelin-1, causing an increase in maternal systemic vascular
resistance in an attempt to improve placental
perfusion.3 Inflammatory mediators such as tumor necrosis factor-alpha and interleukin-6 are
also secreted which drive maternal hypertension, endothelial dysfunction, and oxidative
stress. Cerebral edema and hypertension can result 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 pressures which elicited clinical signs of hypertension such as headache, scotomata, and pulmonary 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
BRIEF REPORTS
Figure 2. Hypertrophic decidual vasculopathy and infarction of spiral
placental arteries in preeclamptic placental tissue.12 Hematoxylin &
eosin (H&E) stain, 100x magnification.
with her first pregnancy (increases the risk 7fold; relative risk 7.19, 95% CI 5.85-8.83), family history of preeclampsia (mother with history
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 absence of diagnostic criteria and then rapid development 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 diagnosis.
Systolic heart failure can result from decompensation of a dilated left ventricle which had previously maintained normal ejection fraction by increasing 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 systemic 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 pulmonary edema. Alveolar macrophages that engulf transudated erythrocytes and proteins are
termed “heart failure cells” (Figure 3).14 The
phenomenon of excess pulmonary arterial pressure 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 postpartum, 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
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PREECLAMPSIA AND PERIPARTUM CARDIOMYOPATHY
Figure 3. Hemosiderin-laden heart failure cells in bronchoalveolar
lavage fluid.15 H&E stain, 40x magnification.
patients compared to pregnant women with nonproteinuric hypertension with similar resting
blood pressure.16
It is important to consider the etiology of peripartum cardiomyopathy in patients presenting
with pneumonia-like vs. transudative symptoms. Our patient was treated ten days post-partum for pneumonia with only normal respiratory
flora cultured. It was atypical, possibly caused
by an imbalance of normal flora within the pulmonary interstitium and a nidus for infection
created by the presence of excess basilar fluid.
The patient’s dyspnea did not resolve upon completion 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 improved markedly. She then developed moderate
mitral regurgitation, mild tricuspid regurgitation, pulmonic insufficiency, and an ejection
fraction of 30%. The ejection fraction during
and after pregnancy had previously been preserved at or above 53%. The patient’s brain natriuretic peptide (BNP) was elevated to 397 pg/
mL at 31 days post-partum, supporting the diagnosis of systolic heart failure.
The patient’s development of systolic heart failure in conjunction with preeclampsia throughout the pregnancy was unexpected but promptly
treated with rapid amelioration of symptoms.
110
This fortunate outcome highlights the importance of close monitoring and integrated continuity of care among the primary care and specialty consulting physicians of the treatment
team. Awareness of potential risks and complications 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 fetus 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 hypertension and preeclampsia to mother and fetus.
The importance of awareness among physicians
of the risks of these clinical features in healthyappearing gravid young women, as well as continuity among primary and specialty care
providers is the key to a safe pregnancy for women 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 cardiomyopathy, which can present with respiratory distress, is a risk associated with preeclampsia.
• Preeclampsia is associated with intrauterine growth retardation that may necessitate
preterm delivery and intrapartum seizure
prophylaxis.
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ACKNOWLEDGEMENTS
8. Maulik D, Yarlagadda P, Youngblood JP, Ciston P. The diagnostic
efficacy of the umbilical arterial systolic/diastolic ratio as a screening
tool: a prospective blinded study. Am J Obstet Gynecol. 1990;162
(6):1518-23.
BRIEF REPORTS
The authors would like to acknowledge the assistance of Dr. Brian Schulte, Dr. Duane Neumann, Dr. Stephen Brierre, Dr. Lance Lamotte,
Dr. Wayne Gravois, Dr. Vincent Shaw, Dr. Brian Benson, and Dr. Kevin Reed in the treatment
of this patient and provision of documents.
7. Steegers EA, Von dadelszen P, Duvekot JJ, Pijnenborg R. Preeclampsia. Lancet. 2010;376(9741):631-44.
9. Hypertension in pregnancy. Report of the American College of
Obstetricians and Gynecologists’ Task Force on Hypertension in
Pregnancy. Obstet Gynecol. 2013;122(5):1122-31.
10. Mustafa R, Ahmed S, Gupta A, Venuto RC. A comprehensive review
of hypertension in pregnancy. J Pregnancy. 2012;2012:105918.
11. Eiland E, Nzerue C, Faulkner M. Preeclampsia 2012. J Pregnancy.
2012;2012:586578.
12. Courtesy of Dr. Beverly Ogden, Woman’s Hospital in Baton Rouge,
La Pathology Dept. and Shannon LaGrange, Compliance Officer,
Pathology Group of Louisiana. Placental infarction of preeclampsia.
6 Dec 2014.
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