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African Health Sciences
Makerere University Medical School
ISSN: 1680-6905 EISSN: 1729-0503
Vol. 11, Num. 1, 2011, pp. 138 - 140
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African Health Sciences, Vol. 11, No. 1, January-March, 2011, pp. 138
- 140
Case report of a 26 year old primigravida with Patent Ductus
Arteriosus (PDA) in heart failure
*Akintunde AA, Opadijo OG
Division of Cardiology, LAUTECH Teaching Hospital, Osogbo, Osun State Nigeria
*Correspondence author: Dr. Akintunde A Adeseye, Department of Medicine,
LAUTECH Teaching Hospital, P.M.B 5000, Osogbo, Osun State, Nigeria, Tel. +234-
803-393-2076, E-mail address: iakintunde2@yahoo.com, iakintunde2@daad-alumni.de
Code Number: hs11021
Abstract
Congenital heart disease is an important cause of maternal morbidity and mortality during pregnancy. Pregnancy alters
the circulatory and respiratory physiology with attendant deleterious effect on the mother with congenital heart disease and
the foetus. Additional insult to the circulatory physiology by other factors coexisting together with congenital heart disease
can further reduce the cardiac reserve in pregnancy and precipitate heart failure. These factors include anaemia,
thromboembolism, hypertension, multiple pregnancy, strenuous physical activity, extremes of temperature and the normal physiological
edema of pregnancy.
Patent ductus arteriosus (PDA) can present for the first time in pregnancy. Moderate to large PDA result in
significant volume overload, left ventricular dilation and dysfunction. In the woman with a hemodynamically important PDA,
pregnancy may precipitate or worsen heart failure. We report a successful pregnancy in a 26 year old primigravida with
previously undetected patent ductus arteriosus with preeclampsia who presented in heart failure. This case highlights the
importance of intensive careful examination of pregnant patients to identify such conditions.
Introduction
Congenital heart disease is an important cause
of maternal morbidity and mortality during
pregnancy.1,2 Hypertensive disorders is also associated
with significant morbidity and mortality in pregnancy
in comparable proportion to the general
population.3 Pregnancy alters the circulatory and
respiratory physiology with attendant deleterious effect on
the mother with congenital heart disease and the
foetus.4
The cardiac reserve of the pregnant woman
with congenital heart disease is already reduced.
Therefore additional insult to the circulatory physiology
by other factors coexisting together with congenital
heart disease can further reduce the cardiac reserve
in pregnancy and precipitate heart failure. These
factors include anaemia, thromboembolism,
hypertension, multiple pregnancy, strenuous physical
activity, extremes of temperature and the normal physiological edema of pregnancy. This oedema
is associated with increase in total exchangeable sodium and water4. The ductus arteriosus derives from
the left sixth primitive aortic arch and connects
the proximal left pulmonary artery to the
descending aorta, just distal to the left subclavian artery.
Functional closure of the ductus from vasoconstriction occurs
shortly after a term birth. Isolated patent
ductus arteriosus (PDA) are categorized based on the
degree of left to right shunting as mild, moderate and
severe PDA which can be subsequently complicated
with Eisemengers complex when there is reversal of shunting with progression to pulmonary
hypertension. Moderate to large PDA result in significant
volume overload, left ventricular dilation and
dysfunction associated with atrial fibrillation and
pulmonary hypertension. Pregnancy is well tolerated in
women with silent and small PDA or in patients who
were asymptomatic before pregnancy. In the woman
with a hemodynamically important PDA, pregnancy
may precipitate or worsen heart failure. Pregnancy
is contraindicated in Eisenmenger syndrome because of the high maternal (e"50 percent) and fetal
(e"60 percent) mortality3,4.
We report a successful pregnancy in a 26 year
old primigravida with previously undetected patent ductus arteriosus with preeclampsia who
presented in heart failure.
Case report
A 26 year old booked primigravida , who had
been apparently well until few weeks earlier when
she presented in the hospital with a history of
progressive dyspnoea on exertion, orthopnoea,
paroxysmal nocturnal dyspnoea and bilateral leg swelling.
Her estimated gestational age was 35 weeks and she
was not a previously diagnosed hypertensive patient.
There was no history of light flashes or epigastric
pain. There was no history to suggest significant left
to right shunting in childhood. Examination revealed
a young woman in a respiratory distress with respiratory rate of 32 cycles per minute, not
clinically pale, afebrile, (Temperature - 36.8 0C). She was well hydrated but had bilateral pitting pedal oedema
up to the knees. Examination of the chest revealed
fine bibasal crepitations. In the cardiovascular system,
the pulse rate was 72 beats per minute, regular and
large volume. Blood pressure was 200/90mmHg.
Jugular venous pressure was elevated. There was
hyperactive precordium and the apex beat was displaced to
the 6th intercoastal space almost at the anterior
axillary line. Heart sounds were S1S2S3 with a gallop
rhythm, a grade 4/6 continuous murmur heard best at
the second intercostal space. Abdominal
examination revealed a uniformly enlarged abdomen with
gravid uterus, fundal height was 35cm and the foetus
was in longitudinal lie and cephalic presentation.
Urinalysis revealed significant proteinuria (+++). Echocardiography revealed dilated left atrial
and ventricular chambers (LAD - 5.2cm,
LVIDd-6.6cm) with systolic dysfunction (Ejection fraction-
40%, Fractional shortening- 24%).There was a
patent ductus arteriosus connecting the left
pulmonary artery with the descending aorta. Peak
pulmonary systolic velocity was 1.0m/s (normal) while the
peak aortic systolic velocity was 1.9m/s
(minimally elevated) .There was no echocardiographic sign
of pulmonary hypertension (peak pulmonary systolic pressure was normal). Electrocardiography
revealed left atrial abnormality, left ventricular
hypertrophy and non specific ST-T wave changes. She
was managed conservatively with antifailure
regimen including strict bed rest, antibiotics, mild
diuresis (Frusemide), reduction in salt intake,
antihypertensive therapy (Methyldopa and Nifedipine) and
continuous fetal monitoring. She had emergency lower
segment caesarean section at 38 weeks of gestation due
to suspected intrauterine growth retardation with
the delivery of a live male foetus, weight 2.6kg,
Apgar score 71105. Postnatal period was not
adversely eventful. She was followed up in the Cardiology Clinic and was thereafter referred to the cardiovascular surgeon for definitive
surgical management.
Discussion
Many haemodynamic changes that occur
normally in pregnancy tend to worsen and
contribute significantly to the morbidity and mortality
in pregnant individuals with already reduced
cardiac reserve such as those with congenital heart
disease.4 Plasma volume increase by as much as 50%
especially in the third trimester. This may possibly explain
why our patient presented with congestive heart
failure at the time she presented. The already
depressed cardiac reserve is further worsened by a
sudden increase in plasma volume, increased total
sodium concentration, anxiety with tachycardia and
other factors such as bacteriuria with associated fever
or any other febrile illness.
There are several factors contributing
to deterioration in cardiovascular status of
pregnant subjects with congestive heart disease.
Hypertensive disorders such as chronic hypertension and
pre-eclampsia are important clinical variables in
this patient. Normally blood pressure falls to about
105/60 mmHg by the mid trimester due to reduction
in peripheral resistance. However increase in
circulatory volume in the third trimester may tilt a
compensated heart into a decompensated stage. Pre-eclampsia
is characterized by proteinuria and elevated blood pressure in a previously normotensive
pregnant woman. The elevated blood pressure is
another triggering factor for decompensation into
the congestive heart failure stage which this
patient presented with. Anxiety especially in a
primigravida can increase the heart rate and also tilt a
compensated heart to a state of decompensation. This may
occur towards the delivery period as she ponders on
the experience of labour.
The main predictors for maternal and
fetal complications in pregnant women with
congenital heart diseases include pulmonary hypertension(pulmonary vascular
disease), maternal cyanosis, poor maternal functional status,
arrhythmias and maternal
anticoagulants.5,6,7,8 The ductus arteriosus connects the descending
aorta to the main pulmonary trunk near the origin of the left
subclavian artery. The physiologic consequences of a PDA
are determined by its size and length as well as by
the ratio of pressure and resistance of the
pulmonary and aortic circulations on either end of the duct.
If systolic and diastolic pressure in the aorta exceeds that in the pulmonary
artery, aortic blood flows continuously down a pressure gradient into the pulmonary
artery and then returns to the left
atrium.8 The left atrium and subsequently the left
ventricle dilate, whereas the right side of the heart
becomes progressively affected as pulmonary
hypertension develops. This will vary with the quantity of
left-to-right shunting as well as with the secondary
effects on the pulmonary vascular bed. Symptoms
generally increase by the second and third decades and
include dyspnea, palpitations, and exercise intolerance.
The incidence of PDA has been noticed to
be increasing over the last two decades due to
improved survival of preterm babies.8 There is a
female predilection,8 and genetic linkage has been
described.9 Individuals with PDA have increased morbidity
and mortality due to heart failure and infective
endocarditis.10 Multiple septic emboli to the
lungs can also occur.
Pregnancies complicated with
Eisemenger complex are at particularly high maternal and
fetal risk with many of them offered termination of
the pregnancy. A successful pregnancy with
Eisemenger complex has however being reported
recently.11 Treatment of the patient may involve surgical
ligation which is the definitive management or by
percutaneous occlusion using cathether based approaches such
as Amplatzer duct occlusion, coil occlusion device
and Rashkind umbrella device.12,13 Pharmacologic treatment using indomethacin or ibuprofen is
useful among preterms but can be complicated by
renal dysfunction.14 The mode of delivery in
pregnant patients with congenital heart disease may be
by vaginal delivery if there is no contraindication to
it and the functional state of the heart is
adjudged adequate. However, in case of any concern
about the functional and / or structural state of the
heart, circulation or the birth canal, induction or
caesarean section as appropriate may be relevant. The
treatment of the preeclampsia involves the use of antihypertensives such as calcium channel
blockers and methyldopa.
Conclusion
This case highlights some points. First,
congenital heart disease can present for the first time
in pregnancy. Secondly, several factors such as
anaemia, hypertension, tachycardia, infection, and
arrhythmias may precipitate acute decompensation in
pregnant subjects with congestive heart disease such as
patent ductus arteriosus. Adequate antenatal
cardiac auscultation screening and appropriate
relevant investigation such as cardiac ultrasound are
important to identify such patients to reduce the
increased morbidity and mortality risk associated with this condition. As subsequent
pregnancies further increase the morbidity, Contraceptive advice should
be offered to such patients immediately postpartum.
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Copyright 2011 - African Health Sciences
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