Case Report KepadaYth.

Non-Infection Unit

PATENT DUCTUS ARTERIOSUS

Presenter : Lasa Dhakka Siahaan (100100071)

Charolina Margaretha (100100255)

Day/Date : Wednesday/ April2nd2014

Supervisor : dr. FeraWahyuni, M.Ked(Ped), Sp.A

Introduction

The patent ductusarteriosus (PDA) is a vascular structure that connects the

proximal descending aorta to the roof of the main pulmonary artery near the

origin of the left branch pulmonary artery. This essential fetal structure

normally closes spontaneously after birth. After the first few weeks of life,

persistence of ductal patency is abnormal. The physiological impact and

clinical significance of the PDA depend largely on its size and the underlying

cardiovascular status of the patient. The PDA may be “silent” (not evident

clinically but diagnosed incidentally by echocardiography done for a different

reason), small, moderate, or large. Regardless of the size, complications may

arise.

Epidemiology

The reported incidence of PDA in term neonates is only 1 in 2,000 births, accounting for 5%-

10% of all congenital heart disease.1 The incidence of PDA in preterm neonates is far greater,

with reports ranging from 20%-60% (depending on population and diagnostic criteria).2 The

increased incidence of PDA in the preterm infant is attributable to the lack of normal closure

mechanisms due to immaturity. Gestational age and weight are intimately linked to PDA in

preterm neonates. Specifically, PDA is present in 80% of infants weighing less than 1,200 g at

birth, compared to 40% of infants weighing less than 2,000 g at birth.1,3Furthermore,

symptomatic PDA is present in 48% of infants with a birth weight of less than 1,000 g.4

Approximately 80% of preterm infants presenting with respiratory distress syndrome (RDS) also

have a PDA,5 which may be due to the increased circulating prostaglandins (PGE2) associated

with RDS.6 Several birth factors have been shown to increase the incidence of PDA, including

high altitude at birth,7 genetic factors,8 and in utero exposure to rubella. 9 For reasons that have

not been elucidated, PDA is more common among female infants than males

(2:1).5Hemodynamically significant PDAs have been associated with significant morbidity and

mortality, which can be as high as 30%.5 This is particularly of concern in preterm neonates, as

they are already at risk for other serious complications. An understanding of the mechanisms

involved, early identification of PDA, and knowledge of therapeutic options are paramount for

successful outcomes.

Pathophysiology

The DA is derived from the distal dorsal sixth aortic arch and is completely formed by the eighth

week of gestation.1Its role is to shunt the blood from the nonfunctional fetal lung through its

connection between the main pulmonary artery and the proximal descending aorta. This right-to-

left shunt allows the blood with a relatively low oxygen concentration to be carried from the

right ventricle through the descending aorta and eventually to the placenta, where gas exchange

will occur. Before birth, approximately 90% of right ventricular output flows through the DA.

Figure 1 illustrates the role of the DA in redirecting fetal circulation in comparison to neonatal

circulation. 10 Premature closure in the fetus is associated with significant morbidities, including

right-sided heart failure, which may result in fetal hydrops.1Normally, the DA closes within 24-

72 hours after a full-term birth; if after 72 hours the ductus fails to close, a diagnosis of persistent

PDA may be made.11,12

The patency of the DA is primarily controlled by low fetal oxygen tension and the

circulation of prostanoids produced from the metabolism of arachidonic acid by COX, with

PGE2 producing the most profound ductal relaxation among the prostanoids.12,13Smooth Muscle

relaxation of the DA results from the activation of the Gcoupled prostaglandin receptor EP 4 by

PGE2. Following the activation of prostaglandin receptor EP4, a cascade of events ensues, which

includes the accumulation of cyclic adenosine monophosphate, increased protein kinase A, and

finally, decreased myosin light chain kinase, leading to vasodilation and ultimately DA

patency.10circulating PGE2 and PGI2 levels are high in the fetus because of production by the

placenta and decreased metabolism in the fetal lungs. The preterm ductus is especially sensitive

to the vasodilatory effects of prostaglandins, contributing to the failure of ductal closure.14 In

term infants, as birth approaches, decreased sensitivity of the DA to prostaglandins and

decreased circulating levels of PGE2 contribute to DA closure.15 Within 24-72 hours after a full-

term birth, the DA closes as a result of increased oxygen tension and decreased circulating PGE2

and prostacyclins (PGI2). As oxygen tension increases, smooth muscle voltage-dependent

potassium channels are inhibited. Through this inhibition, an influx of calcium contributes to

ductal constriction. This oxygen-induced constriction fails in preterm infants potentially due to

immaturity of oxygen-sensing receptors. 16 Levels of circulating PGE2 and PGI2 are decreased as

a result of increased metabolism in the newly functioning lung, as well as the removal of the

placental source. The decreased circulating levels of these potent vasodilators allow the DA to

constrict. These factors collectively contribute to smooth muscle constriction, leading to

ischemic hypoxia of the inner muscle wall of the DA. Functional complete closure usually

occurs within 24 to 48 hours of birth in term neonates. Within the next 2 to 3 weeks, infolding of

the endothelium along with subintimal disruption and proliferation result in fibrosis and a

permanent seal.17The resulting fibrous band with no lumen persists as the ligamentumarteriosum.

Left to Right Shunting

Left-to-right shunting through the ductusarteriosus results in pulmonary overcirculation and left

heart volume overload. Increased pulmonary flow from the ductal shunting leads to increased

pulmonary fluid volume, and in patients with moderate or large shunts, this causes decreased

lung compliance, which may result in increased work of breathing. Pulmonary edema is

uncommon but may occur in older patients with advanced congestive heart failure.1

Increased flow returning to the left heart results in increased left atrial and left ventricular

end-diastolic pressures.The left ventricle compensates by increasing stroke volume and

eventually may hypertrophy to normalize wall stress.Neuroendocrine adaptations also occur,

with increased sympathetic activity and circulating catecholamines that result in increased

contractility and heart rate. The diastolic blood pressure in the aorta decreases owing to diastolic

“runoff”through the patent ductus and, coupled with shorter diastolic time due to tachycardia,

increased intramyocardial tension from left ventricular dilatation, and increased myocardial

oxygen demand, may result in subendocardial ischemia.18

Clinical Presentation

Medical History

The clinical history of patients with PDA varies from thosewho are completely asymptomatic to

those with severecongestive heart failure or Eisenmenger’s syndrome. Manypatients present for

evaluation of an asymptomatic heartmurmur. Others are detected incidentally by an

echocardiogramperformed for another purpose in patients with no overtclinical manifestations.

Some patients may be relatively wellbut report exercise intolerance or have the diagnosis

ofreactive airways disease. Although most patients with PDAcompensate well even with a

moderate left-to-right shunt andremain asymptomatic during childhood, many years ofchronic

volume overload may lead to symptoms of congestiveheart failure in adulthood. Symptoms may

begin withonset of atrial fibrillation that results from chronic andgradually progressive left atrial

enlargement. A previouslywell-tolerated PDA may become clinically significant whenits effects

are combined with acquired conditions such asischemic heart disease or calcific aortic

stenosis.Increased pulmonary flow from the ductal shunting leads to increased pulmonary fluid

volume, and in patients with moderate or large shunts, this causes decreased lung compliance,

which may result in increased work of breathing.1

Physical Examination

The physical examination findings vary as much as themedical history. Patients with tiny,

incidentally discoveredpatent ductus have no abnormal physical findings. Thehallmark physical

finding is a continuous murmur, located atthe upper left sternal border, often referred to as a

“machinery”murmur. The murmur often radiates down the left side ofthe sternum and into the

back, and a thrill may be present.Occasionally a diastolic rumble is audible at the cardiac apexin

patients with moderate or large ductal shunts. If the shuntis moderate or large, the left ventricular

impulse will beprominent, and the pulse pressure will be increased. Theperipheral pulses may be

prominent or bounding. Except inolder patients with congestive heart failure, rales are

uncommoneven with a large shunt.1

Chest Radiograph

Depending on the amount of ductal shunting, the chest radiograph may be completely normal or

it may demonstratecardiomegaly (specifically with signs of left atrial and left ventricular

enlargement) with increased pulmonary vascular markings. The main pulmonary artery is

frequently enlarged, and particularly in older adults with pulmonary hypertension, calcification

of the ductus may be evident.1

Electrocardiogram

The ECG may demonstrate sinus tachycardia or atrial fibrillation, left ventricular hypertrophy,

and left atrial enlargement in patients with moderate or large ductus shunts. In patients with

smaller ductal shunts, the ECG is often completely normal. In the patient with a large

ductusarteriosus and elevated pulmonary artery pressure, signs of right atrial enlargement and

biventricular hypertrophy are frequently present.1

Echocardiogram

The echocardiogram is the procedure of choice to confirm the diagnosis and to characterize a

PDA (Figure 2). In conjunction with the clinical information, the echocardiogram is often useful

in classifying the PDA as silent, small, moderate, or large. In addition to evaluating the

ductusarteriosus, the echocardiogram is used to identify and evaluate other associated cardiac

defects.1

M-mode echocardiography is used to measure the cardiac chamber sizes and quantitate

left ventricular systolic function. In a patient with a small ductusarteriosus, chamber sizes are

usually normal, although mild left atrial and or left ventricular enlargement may be present. In a

patient with a moderate or large patent ductus, the left atrium and left ventricle are enlarged.

Two-dimensional imaging demonstrates the geometry of the ductus. Color Doppler is a very

sensitive modality in detecting the presence of a PDA and is frequently used to estimate the

degree of ductal shunting. Even an extremely tiny patent ductus can be detected by a color flow

signal entering the pulmonary artery near the origin of the left pulmonary artery. In patients with

high pulmonary vascular resistance and PDA, with low velocity or right-to-left flow, the

ductusarteriosus may be very difficult to demonstrate with color flow Doppler, even if it is large.

Findings such as septal flattening, unexplained right ventricular hypertrophy, and high-velocity

pulmonary regurgitation should prompt a thorough investigation for a PDA. Contrast

echocardiography may be helpful in this setting; intravenous injection of agitated saline leads to

microbubbles in the descending aorta (from ductal right-to-left shunting) but not in the ascending

aorta.1

A complete pulmonary artery pressure curve can be generated from the spectral Doppler

signal of ductal flow.19Theright ventricular pressure can be estimated from the peak velocity of

the tricuspid regurgitation jet, if present. TheDoppler velocity of the pulmonary regurgitation

flow, if present, can be used to estimate the pulmonary artery diastolic pressure. With the

outflow tract cross-sectional areas and Doppler-derived mean flow velocities, the degree of left-

toright shunt can be calculated.

Figure 2.Echocardiogram study demonstrating PDA.

A, Twodimensional image of a PDA as seen in a high parasternal shortaxis view. DAO indicates descending aorta; MPA, main pulmonary artery. B, Color Doppler image in a similar view shows leftto- right shunting through the ductus. C, Spectral Doppler profile of continuous left-to-right ductal flow.

Magnetic Resonance Imaging and ComputedTomography

In the adult with PDA, computed tomography can assess the degree of calcification,20 which may

be important if surgical therapy is considered. Magnetic resonance imaging and computed

tomography may be useful in defining the anatomy in patients with unusual PDA geometry and

in patients with associated abnormalities of the aortic arch.21 One example is the patient with

ductusarteriosus aneurysm, which may present as a chest mass.22,23Other examples include PDA

associated with vascular ring, with right aortic arch, and with cervical arch.

Cardiac Catheterization

Therapeutic catheterization is currently the treatment of choice at most centers for most children

and adults withpatent ductus. Complete diagnostic assessment of hemodynamics before

transcatheter closure is particularly importantin adults with patent ductus, in whom it is

imperative to fully evaluate the pulmonary vascular resistance and degree of shunting before

intervention. In patients with elevated pulmonary artery pressure, assessment of pulmonary

vascular resistance and its response to vasodilating agents such as oxygen, nifedipine,

prostacyclin, sildenafil, and nitric oxide may be helpful in determining advisability of ductus

closure. Assessment of hemodynamics during temporary test occlusion with a balloon catheter

may also provide important information regarding advisability of closure. Angiography defines

the anatomy of the ductusarteriosus. Detailed assessment of the ductal anatomy is essential

before transcatheter closure so that the proper device and device size can be chosen for the

intervention. Important features include the minimum diameter, the largest diameter (usually at

the aortic ampulla), the length, and the relationship of the ductus to the anterior border of the

tracheal shadow, which helps guide device positioning.1

Treatment

Medical Management

Symptomatic patients with PDA usually improve with a medical regimen of diuretics and

digoxin. Afterload reduction, such as with angiotensin-converting enzyme inhibition, may also

affect clinical improvement, although definitive studies in this setting are not available.

Antidysrhythmia medications may be useful in patients with atrial fibrillation or flutter, and

although some patients may be successfully cardioverted and maintained in sinus rhythm after

closure of the ductus, adults with atrial fibrillation may require therapy indefinitely, including

anticoagulation. Observance of infective endocarditis prophylaxis precautions is recommended

for all patients with PDA, including those with silent PDA, until 6 months after closure. Medical

therapy for congestive heart failure due to PDA may be short-term, until definitive surgical or

transcatheter closure is performed, but may also be required long-term in patients with

cardiomegaly and persistent symptoms.1

Patients with PDA and pulmonary vascular disease whoare considered unacceptable

candidates for definitive closure may be managed with pulmonary vasodilating agents such as

chronic oxygen, PGI2, calcium channel blockers, endothelin antagonists, and phosphodiesterase

type V inhibitors. One strategy in such patients is to accomplish partial closure of the ductus by

surgery or transcatheter techniques, to make it “restrictive” but not completely closed, followed

by longterm therapy with pulmonary vasodilating agents. If in follow-up, the pulmonary vascular

resistance decreases, then complete closure may be considered. Systematic study of the benefits

of pulmonary vasodilating agents in the setting of PDA and high pulmonary vascular resistance

are not available, however, and such treatment strategies are unproved and results anecdotal at

the present time.1

Indications for Closure of PDA

Ductus closure is clearly indicated for any child or adult who is symptomatic from significant

left-to-right shunting through the PDA. In asymptomatic patients with significant left-toright

shunting that results in left heart enlargement, closure is indicated to minimize the risk of

complications in the future.24 In adults with PDA, reported outcomes after PDA closure have

been very good, including for those with modest elevation in pulmonary vascular resistance and

even some with Eisenmenger’s syndrome.25 Elimination of the shunt reduces pulmonary blood

flow, and therefore pulmonary artery pressure.

The indications for closure of patent ductus with small shunts, including those that are tiny and

incidentally discovered (“silent”), are less certain, particularly in older adults. Because closure

methods are effective and safe and are associated with minimal morbidity, a strategy advocating

routine closure of any PDA in children and young adults appears most reasonable.

Transcatheter Closure

Transcatheter occlusion has become the treatment of choice for most patent ductus in children

and adults. In cases ofcalcified ductusarteriosus with increased pulmonary vascular resistance,

transcatheter closure offers considerable advantages over surgical closure, which frequently

involves cardiopulmonary bypass with an anterior approach through a median sternotomy. The

basic technique is to advance a catheter or delivery sheath across the ductusarteriosus from either

the pulmonary artery or the aorta and position a closure device in the ductus to occlude it.

Results of transcatheter occlusion of PDA have been excellent. Complete closure rates at follow-

up generallyexceed 90% to 95% in most studies.26 As a result of device modifications, evolution

of new techniques, and increasedoperator skill, success rates for complete closure have improved

significantly over time. Even when a small residualshunt is detected at follow-up, complete

occlusion can usually be achieved by delivery of a single small additional coil. Serious

complications of transcatheter closure of the patent ductus are rare. The most common

complication is device embolization, which was relatively common early in the experience with

coils. Embolized coils are usually retrieved, but even in cases in which they cannot be retrieved,

adverse consequences are rare. Other potentially important complications are flow disturbance in

the proximal left pulmonary artery or descending aorta from a protruding device, hemolysis from

high-velocity residual shunting, femoral artery or vein thrombosis related to vascular access, and

infection.

Surgical Therapy

Although generally associated with greater pain and morbidity than transcatheter methods,

surgical ligation and surgical division are safe and effective procedures that historically have set

a high standard by which transcatheter techniques have been judged. Surgical ligation or division

of the PDA remains the treatment of choice for the rare very large ductus. Rarely, a large,

window-type PDA may have insufficient length to permit ligation, and the appropriate surgical

procedure is patch closure on cardiopulmonary bypass.27 Complete closure rates of surgical

ligation (often accompanied by division of the ductus) in published reports range from 94% to

100%, with 0% to 2% mortality.28 Important complications include bleeding, pneumothorax,

infection, and rarely, ligation of the left pulmonary artery or aorta. Surgical morbidity, cost, and

hospital length of stay have been decreased with use of transaxillary muscle-sparing

thoracotomy29 and by the technique of video-assisted thoracoscopicsligation of the PDA.30

The aim of this paper is to report a case of patent ductus arteriosus in a 11 years old girl.

Case

Name : RAR

Age :11 years

Sex : Female

Date of Admission : March, 3rd 2014

Main Complaint: shortness of breathing

History: shortness of breathing presents since 5 months ago. Worsening for a week for the

patient did not consume the drugs regularly.Shortness of breath increase in activities and

decrease when patient take a rest.

History of fever (+) since 1 month ago, Moderate fever relieve with antipyretics drugs, seizure

(-), shiver (-).

History of previous illness : intermitten cough (+) for a month with no sputums,had a previous

consultation from dr.Tina,SpA(k) and diagnosed with moderate PDA+ mild Aorta Insufficiency+

mild mitral insufficiency (echo’s result on November 2013)

History of previous medications:getting prescribe withlasix 2x 20 mg and Aldacton 2 x 12,5

mg for 3 months, but the consumption of Aldacton had stop a week ago because Aldacton was

unavailable in their village

History of labor :.normal delivery, at home, helped by midwife,cried as soon as

baby was born, no cyanosis

History of feeding :breast milk until 11 months

History of immunization :complete immunization

Presens status

Sensorium : Compos Mentis Anemis : -

Body temperature : 37,6oC Icteric : -

Respiratory Rate : 32 x/minute Cyanosis : -

Pulse : 126 bpm Dyspnea : +

Physical Examination

weight : 20 kg BW/Age: 52.6 %

height: 139 cm BH/Age: 96.5%

Upper Arm Circumference (UAC):14 cm BW/BH: 58.8 %

Abdomen Circumference (AC) : 53 cm

1. Head: Eye: light reflexes(+/+), isocor pupil, pale conjunctiva palpebra inferior (-/-),

icteric (-/-), Ear : normal, Nose: normal, Mouth: normal,

2. Neck: Lymph node enlargement (-), cannon wave (+), TVJ R+ 0 cmH2O

3. Thorax : Symmetrical fusiformis, retraction (-)

HR: 126 bpm, regular, continous murmur (+), ICR III-IV

RR: 32 x/minute, regular, crackles (-/-), wheezing (-)

Abdomen: soepel, peristaltic (+) normal,liver: palpable 4 cms below the right

arcus costa, Spleen/Renal: not palpable, Anogenital : female, Anus (+)

4. Extremities: Pulse 126 bpm, regular, adequate vascular pressure and volume,

warmacral, CRT< 3”, swelling (+), BP : 100/60 mmhg

Working Diagnosis

Congestive Heart Failure ec moderate Patent Ductus Arteriosus+ mild Mitral Insufficiency+ mild

Aorta insufficiency

Treatment

O2 1-2 L/minute nasal canule

IVFD D5% Nacl 0,45% 4 gtt/minute micro

Follow up on March 4th 2014

S : shortness of breathing (+)

O: Sensorium: ComposMentis, Body temperature: 37,6oC, RespiratoryRate: 32x/minute, Pulse:

126 bpm,Anemis (-),Icteric (-),Cyanosis(-),Dyspnea(+),Weight: 20 kg, Height: 139 cm, UAC :

14 cm, AC:

Head : Eye: light reflexes(+/+), isocor pupil, pale conjunctiva

palpebrainferior (-/-), icteric (-/-), Ear : normal, Nose:

normal, Mouth: normal

Neck : Lymph node enlargement (-), cannon wave (+), TVJ R+ 0 cmH2O

Thorax : Symmetrical fusiformis, retraction (-),HR: 126 bpm, regular,

continous murmur (+), ICR III-IV,RR: 32 x/minute, regular, crackles

(-/-), wheezing (-)

Abdomen: soepel, peristaltic (+) normal,liver: palpable 4 cms below

the right Arcus costa, Spleen/Renal: not palpable,

Anogenital : female, Anus (+)

Extremities : Pulse 126 bpm, regular, adequate vascular pressure and volume,

warmacral, CRT< 3”, BP : 100/60 mmhg

A : Congestive Heart Failure ec moderate Patent Ductus Arteriosus+mild Mitral Insufficiency+

mild Aorta insufficiency

P:

Furosemide inj. 20 mg/12 hrs/IV

Spironolacton 2x12.5 mg

Captopril 2x625 mg

Regular diet low salt 1500 kkal+40 gr Protein

Laboratory findings on March 4th 2014:

Blood gases analysis : PH 7.493,pCO2 20.5 mmHg,pO2 186.7 mmHg,Bicarbonat 15.3 mmol/L,

total CO2 16.0 mmol/L, BE -7.3 mmol/L, O2 saturation 98.3

Carbohydrate metabolism : Random blood glucose 106.20 mg/dL

Electrolyte : Na 131 mEq, K 3.7 mEq, Cl 110 mEq

Complete Blood Count : HGB 5.70 g%, RBC 2.21 106/mm3, WBC 12.68 106/mm3, haematocryte

18.40 %,Trombocyte 100 106/mm3, MCV 83.30 fL, MCH 25.80 pg, MCHC 31 g%, RDW 20.90

%, MPV 10 fL, PCT 0.10 %, PDW 11.8 fL, Neutrophil 75.90 %, lymphocyte 13.70 %, monocyte

9.60 %, eosinophil 0.60 %, basophil 0.200 %, Absolute neutrophil 9.63 106/µL, Absolute

lymphocyte 1.74 106/µL, Absolute monocyte 1.22 106/µL, Absolut eosinophil 0.07 106/µL,

Absolute basophil 0.02 106/µL.

Consultation results fromcardiology department on March4th 2014:Echocardiography’s result: Moderate Patent Ductus Arteriosus + Mild PE + Vegetation of

Pulmonary valve+ mild Mitral Insufficiency+mild tricuspid insufficiency+mild pulmonary

insufficiency

ECG’s results : Sinus Tachycardi, T wave abnormality consider anterior ischemia, abnormal

ECG

Advices : Check for Albumin, Transfusion if Hb <8 mg.dl,repeat the echocardiography to see

endocarditis sign,furosemide inj,spironolacton,captopril, regular diet low salt.

Follow up on March 6th-7th March

S : shortness of breathing (+)

O: Sensorium: ComposMentis, Body temperature: 37,6oC, RespiratoryRate: 32x/minute, Pulse:

126 bpm,Anemis (-),Icteric (-),Cyanosis(-),Dyspnea(+),Weight: 20 kg, Height: 139 cm, UAC :

14 cm, AC:

Head : Eye: light reflexes(+/+), isocor pupil, pale conjunctiva

palpebrainferior (-/-), icteric (-/-), Ear : normal, Nose:

normal, Mouth: normal

Neck : Lymph node enlargement (-), cannon wave (+), TVJ R+ 0 cmH2O

Thorax : Symmetrical fusiformis, retraction (-),HR: 126 bpm, regular,

continous murmur (+), ICR III-IV,RR: 32 x/minute, regular, crackles

(-/-), wheezing (-)

Abdomen: soepel, peristaltic (+) normal,liver: palpable 4 cms below

the right Arcus costa, Spleen/Renal: not palpable,

Anogenital : female, Anus (+)

Extremities : Pulse 126 bpm, regular, adequate vascular pressure and volume,

warmacral, CRT< 3”, BP : 100/60 mmhg

A : Congestive Heart Failure ec moderate Patent Ductus Arteriosus+ mild PE+ vegetation of

pulmonary valve+mild Mitral insufficiency+ mild Tricuspid Insufficiency+ mild

Pulmonary insufficiency

P: Total bed rest

Semi fowler position

O2 1-2 L/minutes nasal canule

Ceftriaxone injection 1000 mg/12 hour/IV (day 2)

Gentamycin injection so mg/12 hour/ (day 2)

Furosemide injection 20 mg/12 hour/IV

Spironolacton 2x12,5 mg

Captopril 2x6,25 mg

Regular diet low salt 1500 kkal + 40 gr protein

Fluid balance every 6 hours

PRC transfusion 60 cc B+

Follow up on March 8th 2014

S : shortness of breathing (+)

O: Sensorium: Compos Mentis, Body temperature: 37.0oC ,

RespiratoryRate:32x/minute,Pulse: 118 bpm,Anemis (-),Icteric (-),Cyanosis(-),Dyspnea(+),

Weight: 20 kg, Height: 139 cm, UAC : 14 cm

Head :Eye: light reflexes(+/+), isocor pupil, pale conjunctiva palpebrainferior (-/-),

icteric (-/-), Ear : normal, Nose: normal, Mouth: normal

Neck : Lymph node enlargement (-),TVJ R+ 0 cmH2O

Thorax : Symmetrical fusiformis, retraction (-), Ictus (+), thrill(+)

HR: 100 bpm, regular, continous murmur (+) grade 4/6 lower mid

clavicula sinistra ICR IV-V, RR: 30 x/minute, regular, crackles

(-/-), wheezing (-)

Abdomen: soepel, peristaltic (+) normal,liver: palpable 4 cms below

the right Arcus costa, Spleen/Renal: not palpable,

Anogenital: female, Anus (+)

Extremities: Pulse 100 bpm, regular, adequate vascular pressure and volume,

warmacral, CRT< 3”, BP : 100/60 mmhg

A : Congestive Heart Failure ec moderate Patent Ductus Arteriosus+ mild PE+ vegetation of

pulmonary valve+mild Mitral insufficiency+ mild Tricuspid Insufficiency+ mild

Pulmonary insufficiency

P: Total bed rest

Semi fowler position

O2 1-2 L/minutes nasal canule

Ceftriaxone injection 1000 mg/12 hour/IV (day 2)

Gentamycin injection so mg/12 hour/ (day 2)

Furosemide injection 20 mg/12 hour/IV

Spironolacton 2x12,5 mg

Captopril 2x6,25 mg

Regular diet low salt 1500 kkal + 40 gr protein

Fluid balance every 6 hours

PRC transfusion 60 cc B+

Follow up on March 9th -10th 2014

S:shortness of breathing (+), cough (+), fever (+)

O:Sensorium: Compos Mentis, Body temperature: 37.9oC ,

RespiratoryRate:32x/minute,Pulse: 118 bpm,Anemis (-),Icteric (-),Cyanosis(-),Dyspnea(+),

Weight: 20 kg, Height: 139 cm, UAC : 14 cm

Head :Eye: light reflexes(+/+), isocor pupil, pale conjunctivapalpebrainferior (-/-),

icteric (-/-), Ear : normal, Nose: normal, Mouth: normal

Neck : Lymph node enlargement (-),TVJ R+ 0 cmH2O

Thorax : Symmetrical fusiformis, retraction (-), Ictus (+), thrill(+)

HR: 100 bpm, regular, continous murmur (+) grade 4/6 lower mid

clavicula sinistra ICR IV-V, RR: 30 x/minute, regular, crackles

(-/-), wheezing (-)

Abdomen: soepel, peristaltic (+) normal,liver: palpable 4 cms below

the right Arcus costa, Spleen/Renal: not palpable,

Anogenital: female, Anus (+)

Extremities: Pulse 100 bpm, regular, adequate vascular pressure and volume,

warmacral, CRT< 3”, BP : 100/60 mmhg

A : Congestive Heart Failure ec moderate Patent Ductus Arteriosus+ mild PE+ vegetation

of pulmonary valve+mild Mitral insufficiency+ mild Tricuspid Insufficiency+ mild Pulmonary

insufficiency

P: Total bed rest

Semi fowler position

O2 1-2 L/minutes nasal canule

Ceftriaxone injection 1000 mg/12 hour/IV (day 2)

Gentamycin injection so mg/12 hour/ (day 2)

Furosemide injection 20 mg/12 hour/IV

Spironolacton 2x12,5 mg

Captopril 2x6,25 mg

Reguler diet low salt 1500 kkal + 40 gr protein

PRC transfusion 60 cc (9th)and 100 cc (10th)

Follow up on March 11th-13th 2014

S:shortness of breathing (+), cough (+), fever (+)

O:Sensorium: Compos Mentis, Body temperature: 38.2oC ,

RespiratoryRate:32x/minute,Pulse: 118 bpm,Anemis (-),Icteric (-),Cyanosis(-),Dyspnea(+),

Weight: 20 kg, Height: 139 cm, UAC : 14 cm

Head :Eye: light reflexes(+/+), isocor pupil, pale conjunctivapalpebrainferior (-/-),

icteric (-/-), Ear : normal, Nose: normal, Mouth: normal

Neck : Lymph node enlargement (-),TVJ R+ 0 cmH2O

Thorax : Symmetrical fusiformis, retraction (-), Ictus (+), thrill(+)

HR: 100 bpm, regular, continous murmur (+) grade 4/6 lower mid

clavicula sinistra ICR IV-V, RR: 30 x/minute, regular, crackles

(-/-), wheezing (-)

Abdomen: soepel, peristaltic (+) normal,liver: palpable 4 cms below

the right Arcus costa, Spleen/Renal: not palpable,

Anogenital: female, Anus (+)

Extremities: Pulse 100 bpm, regular, adequate vascular pressure and volume,

warmacral, CRT< 3”, BP : 100/60 mmhg

A : Congestive Heart Failure ec moderate Patent Ductus Arteriosus+ mild PE+ vegetation

of pulmonary valve+mild Mitral insufficiency+ mild Tricuspid Insufficiency+ mild Pulmonary

insufficiency

P: Total bed rest

Semi fowler position

O2 1-2 L/minutes nasal canule

Ceftriaxone injection 1000 mg/12 hour/IV (day 2)

Gentamycin injection so mg/12 hour/ (day 2)

Furosemide injection 20 mg/12 hour/IV

Spironolacton 2x12,5 mg

Captopril 2x6,25 mg

Reguler diet low salt 1500 kkal + 40 gr protein

Ambroxol syr 3x 1 cth

Balance every 6 hours

Dipstick result (12th March 2014)

Leu Nit Uro Pro PH BLO SG Ket Bil Glu

- + 0.2(3x) 15(0.15)± 5.0 +++ 1.020 - - -

Follow up on March 14th-20th 2014

S:shortness of breathing (+), cough (+), fever (-)

O:Sensorium: Compos Mentis, Body temperature: 37.2oC , Respiratory Rate:36 x/minute,

Pulse: 112bpm, Anemis (-),Icteric (-),Cyanosis(-),Dyspnea(+), Weight: 20 kg, Height: 139 cm,

UAC : 14 cm, BP: 100/50 mmhg

Head : Eye: light reflexes(+/+), isocor pupil, pale conjunctiva

palpebrainferior (-/-), icteric (-/-), Ear : normal, Nose: normal, Mouth: normal

Neck : Lymph node enlargement (-),TVJ R+ 0 cmH2O

Thorax : Symmetrical fusiformis, retraction (-), Ictus (+), thrill(+)

HR: 100 bpm, regular, continous murmur (+) grade 4/6 lower mid clavicula

sinistra ICR II-III,RR: 22 x/minute, regular, crackles (-/-), wheezing (-)

Abdomen : soepel, peristaltic (+) normal,liver: palpable 4 cms below

the right Arcus costa, Spleen/Renal: not palpable,

Anogenital : female, Anus (+)

Extremities : Pulse 112 bpm, regular, adequate vascular pressure and volume,

warmacral, CRT< 3”, swelling (+), BP : 100/60 mmhg

A : Congestive Heart Failure ec moderate Patent Ductus Arteriosus+ mild PE+ vegetation of

pulmonary valve+mild Mitral insufficiency+ mild Tricuspid Insufficiency+ mild

Pulmonary insufficiency

P: Total bed rest

Semi fowler position

O2 1-2 L/minutes nasal canule

Ceftriaxone injection 1000 mg/12 hour/IV (day 2)

Gentamycin injection so mg/12 hour/ (day 2)

Furosemide injection 20 mg/12 hour/IV

Spironolacton 2x12,5 mg

Captopril 2x6,25 mg

Ambroxol syr 3x 1 cth

Balance every 6 hours

Regular diet low salt 1500 kkal + 40 gr protein

Laboratory findings on March 14th – 20th 2014

Immunoserology : Total T3 0.88ng/ml, Total T4 1.68 µg/ml, TSH 4.890 µIU/ml, qualitative

CRP (+), Procalcitonin 0.36 ng/ml

Electrolyte: Na 130 mEq/L, K 4.6 mEq/L, chloride 97 mEq/L

Complete Blood Count : HGB 11.60 g%, RBC 4.23 106/mm3, WBC 13.35 106/mm3,

haematocryte 35.50 %,Trombocyte 379 106/mm3, MCV 83.90 fL, MCH 27.40 pg, MCHC 32.70

g%, RDW 16.30%, MPV 8.70 fL, PCT 0.33 %, PDW 9.1 fL, Neutrophil 64.50 %, lymphocyte

20.10 %, monocyte 13.90 %, eosinophil 1.00 %, basophil 0.500 %, Absolute neutrophil 8.59

106/µL, Absolute lymphocyte 2.69 106/µL, Absolute monocyte 1.86 106/µL, Absolut eosinophil

0.14 106/µL, Absolute basophil 0.07 106/µL.

Follow up on March21st-24th 2014

S:shortness of breathing start to decrease, the food was not finished, cough(+)

O:Sensorium: Compos Mentis, Body temperature: 37.0oC , Respiratory Rate:34 x/minute,

Pulse: 108bpm, Anemis (-),Icteric (-),Cyanosis(-),Dyspnea(+), Weight: 20 kg, Height : 139

cm, UAC : 14 cm, BP: 100/50 mmhg,BBM: 17.5 kg, BBS: 17.5 kg, LLA : 13 cm

,BW/BH: 67.3%, BW/age : 46.05 %,BH/age: 88.15%

Head : Eye: light reflexes(+/+), isocor pupil, pale conjunctiva

palpebrainferior (-/-), icteric (-/-), Ear : normal, Nose: normal, Mouth: normal

Neck : Lymph node enlargement (-),TVJ R+ 0 cmH2O

Thorax : Symmetrical fusiformis, retraction (-), Ictus (+), thrill(+)

HR: 100 bpm, regular, continous murmur (+) grade 4/6 lower mid clavicula

sinistra ICR II-III

RR: 22 x/minute, regular, crackles (-/-), wheezing (-)

Abdomen : soepel, peristaltic (+) normal,liver: palpable 4 cms below

the right Arcus costa, Spleen/Renal: not palpable, Anogenital : female,

Anus (+)

Extremities : Pulse 100 bpm, regular, adequate vascular pressure and volume,

warmacral, CRT< 3”, swelling (+), BP : 100/60 mmhg

A : Congestive Heart Failure ec moderate Patent Ductus Arteriosus+ mild PE+ vegetation of

pulmonary valve+mild Mitral insufficiency+ mild Tricuspid Insufficiency+ mild

Pulmonary insufficiency+ marasmus type of malnutrition

P: Total bed rest

Semi fowler position

O2 1-2 L/minutes nasal canule

Ceftriaxone injection 1000 mg/12 hour/IV (day 2)

Gentamycin injection so mg/12 hour/ (day 2)

Furosemide injection 20 mg/12 hour/IV

Spironolacton 2x12,5 mg

Captopril 2x6,25 mg

Ambroxol syr 3x 1 cth

Balance every 6 hours

Reguler diet low salt 1500 kkal + 40 gr protein

Diet F100 125 cc/2 jam

Multivitamin without Fe 1x1 cth

Folic acid 1x 5 mg

R/ consule to Departement of Oral and Dental health

Consultation results from cardiology dept : repeat the Echocardiography after 6-8 weeks of

therapy

Culture result:

Throat swab culture: Streptococcus aglactie

Sensitif: Ceftriaxon, levolinezolid,levofloxacin

Resisten: Ampicilin,

azitromicin,erythromycin,clindamicin

Follow up 25th-27th March 2014

S: shortness of breathing (+), cough (+), fever (-),food was finished

O:Sensorium: Compos Mentis, Body temperature: 37.0oC , Respiratory Rate:34 x/minute,

Pulse: 108bpm, Anemis (-),Icteric (-),Cyanosis(-),Dyspnea(+), Weight: 20 kg, Height: 139 cm,

UAC : 14 cm, BP: 100/50 mmhg, BBM : 17.5 kg, UAC : 14 cm ,BH/age : 88.9 %, BBS :18

kg, BW/age: 46.5 %, BW/BH : 70.1 %

Head : Eye: light reflexes(+/+), isocor pupil, pale conjunctiva

palpebrainferior (-/-), icteric (-/-), Ear : normal, Nose: normal, Mouth: normal

Neck : Lymph node enlargement (-),TVJ R+ 0 cmH2O

Thorax : Symmetrical fusiformis, retraction (-), Ictus (+), thrill(+)

HR: 100 bpm, regular, continous murmur (+) grade 4/6 lower mid clavicula

sinistra ICR II-III

RR: 22 x/minute, regular, crackles (-/-), wheezing (-)

Abdomen : soepel, peristaltic (+) normal,liver: palpable 4 cms below

the right Arcus costa, Spleen/Renal: not palpable, Anogenital : female,

Anus (+)

Extremities : Pulse 100 bpm, regular, adequate vascular pressure and volume,

warmacral, CRT< 3”, swelling (+), BP : 100/60 mmhg

A : CHF ec moderate PDA+Mild PE+vegetation of the pulmonary valve+mild tricuspid

insufficiency+mild pulmonal insufficiency+ marasmus+ caries dentis+ ginggival pulpa

P: Bed rest+ semi fowler position

O2 1 liter/minute nasal canule (intermitten)

Furosemide injection 20 mg/12 hours/IV

Spironolacton 2x12.5 mg

Captopril 2x6,25 mg

Ampicilin injection 1 gram/6 hours/IV(day 12)

Gentamycin injection 50 mg/12 hours/IV (day 22)

Ambroxol syrup 3x1 Cth

Folic acid 1x5 mg

Multivitamin without Fe 1x1 cth

regular diet 1000 kkal + fluid consistency diet (F100) 3 x 200 cc

Follow up 28th-29th March 2014

S: shortness of breathing (+), cough (+), fever (-),food was finished

O:Sensorium: Compos Mentis, Body temperature: 37.0oC , Respiratory Rate:34 x/minute,

Pulse: 108bpm, Anemis (-),Icteric (-),Cyanosis(-),Dyspnea(+), Weight: 20 kg, Height: 139 cm,

UAC : 14 cm, BP: 100/50 mmhg, BBM : 17.5 kg, UAC : 14 cm ,BH/age : 88.9 %, BBS :18

kg, BW/age: 46.5 %, BW/BH : 70.1 %

Head : Eye: light reflexes(+/+), isocor pupil, pale conjunctiva

palpebrainferior (-/-), icteric (-/-), Ear : normal, Nose: normal, Mouth: normal

Neck : Lymph node enlargement (-),TVJ R+ 0 cmH2O

Thorax : Symmetrical fusiformis, retraction (-), Ictus (+), thrill(+)

HR: 100 bpm, regular, continous murmur (+) grade 4/6 lower mid clavicula

sinistra ICR II-III

RR: 22 x/minute, regular, crackles (-/-), wheezing (-)

Abdomen : soepel, peristaltic (+) normal,liver: palpable 4 cms below

the right Arcus costa, Spleen/Renal: not palpable, Anogenital : female,

Anus (+)

Extremities : Pulse 100 bpm, regular, adequate vascular pressure and volume,

warmacral, CRT< 3”, swelling (+), BP : 100/60 mmhg

A : CHF ec moderate PDA+Mild PE+vegetation of the pulmonary valve+mild tricuspid

insufficiency+mild pulmonal insufficiency+ marasmus+ caries dentis+ ginggival pulpa

P: Bed rest+ semi fowler position

O2 1 liter/minute nasal canule (intermitten)

Furosemide injection 20 mg/12 hours/IV

Spironolacton 2x12.5 mg

Captopril 2x6,25 mg

Ampicilin injection 1 gram/6 hours/IV(day 12)

Gentamycin injection 50 mg/12 hours/IV (day 22)

Ambroxol syrup 3x1 Cth

Folic acid 1x5 mg

Multivitamin without Fe 1x1 cth

regular diet 1000 kal + fluid consistency diet (F100) 3 x 200 cc

Laboratory findings on March 28th 2014

Complete Blood Count : HGB 12.80 g%, RBC 4.59 106/mm3, WBC 14.68106/mm3,

haematocryte 37 %,Trombocyte 361 106/mm3, MCV 80.6 fL, MCH 27.90 pg, MCHC 34.60 g%,

RDW 15.80%, MPV 8.40 fL, PCT 0.3 %, PDW 8.8 fL,ESR 15 mm/hrs, Neutrophil 64.90 %,

lymphocyte 22.70 %, monocyte 9 %, eosinophil 3.1 %, basophil 0.3 %, Absolute neutrophil

9.52 106/µL, Absolute lymphocyte 3.33 106/µL, Absolute monocyte 1.32 106/µL, Absolut

eosinophil 0.14 106/µL, Absolute basophil 0.07 106/µL.

Immunoserology : CRP positive, procalcitonine 0.12 ng/ml

Discussion

Patient RAR came to Adam malik general hospital with main complaint shortness of breathing

since 5 months ago. RAR have consultated with dr. Tina C.L Tobing, Sp.A(K) and diagnosed

with PDA moderate, mild Aorta Insufficiency,and mild mitral Insufficiency by

echocardiography on november 2013. Since RAR had refered at Adam Malik, RAR diagnosed

with moderate PDA , mild PE , vegetation on pulmonary valve, mild PI, mild TI, mild MI from

echocardiography on 5 march 2014.

This patient had typical clinical manifestation of Patent ductus arteriosus, such as

shortness of breathing from medical history and continous murmur from physical examination.

Shortness of breathing in this patient caused by increased pulmonary flow from patent ductus

arteriosus shunting and leads to increased pulmonary fluid volume. This condition causes

decreased lung compliance, which may result in increased work of breathing. Continuous

murmur or often reffered to as a “machinery” murmur is the hallmark physical finding in PDA.

Murmur located at the upper left sternal border and a thrill may be present. In this patient

continuous murmur and thrill present at the lower mid clavicula sinistra intercostal IV-V so it

classified as grade IV/VI of murmur.

On other physical diagnostic, hepatomegaly is present. This is found by abdomen

palpation, normally liver is not palpable. But in this patient liver is palpable 4cm below arcus

costae dextra. Hepatomegaly in this patient is one of the clinical manifestation from congestive

heart failure. Congestive heart failure in this patient occured for the result of the volume overload

on right side of heart. Increased pressure on right side of heart caused by pulmonary valve

insufficiency, which create a back flow of blood from artery pulmonal and leads to volume

overload on right side of heart. Volume overload caused high pressure on right side of heart and

leads to back flow to superior and inferior cava veins. This condition caused jugular vein high

pressure and hepatomegaly

The diagnosis of moderate PDA was confirmed by echocardiogram. Echocardiogram is

the procedure of choice to confirm the diagnosis and to characterize a PDA. In addition to

evaluating the ductus arteriosus, the echocardiogram is used to identify and evaluate other

associated cardiac defects. In this case mild PE, vegetation on pulmonary valve, mild MI, mild

TI, and mild PI is found as other associated cardiac defects. M-mode echocardiography is used to

measure the cardiac chamber sizes and quantitate left ventricular systolic function. In a patient

with a small ductus arteriosus, chamber sizes are usually normal, although mild left atrial and or

left ventricular enlargement may be present. In a patient with a moderate or large patent ductus,

the left atrium and left ventricle are enlarged. On echocardiogram examination, dilated left

ventricle and left atrium is found in this patient.

RAR is given Furosemid, Spironolactone, Captopril, Ceftriaxone (which is stopped

because of bacterial resistant, and exchange with Ampicillin), and Gentamicin. Furosemid,

spironolactone, and captopril is treatment for congestive heart failure which is complication from

PDA on this patient. This drugs reduce pre-load and after-load in aim to decreased burden of the

heart. Furosemid is Loop diuretics drug, mechanism of action furosemid inhibits reabsorption of

sodium and chloride ions at proximal and distal renal tubules and loop of henle by interfering

with chloride-binding cotransport system, causes excretion increases in water, calcium,

magnesium, sodium and chloride.

Mechanism of action of spironolactone is aldosterone antagonist with diuretic and

antihypertensive effects. Competitive binding of receptors at aldosterone-dependent Na-K

exchange site in distal tubules results in increased excretion of Na+, Cl-, and H2O and retention

of K+ and H+. Aldosterone receptor antagonist medicines may be a good option for people with

heart failure who are already taking other medicines such as ACE inhibitors, other diuretics,

digoxin, and beta blocker.

Captopril perevents the conversion of angiotensin I to angiotensin II (a potent

vasoconstrictor) through inhibition of ACE by competing with physiologic subtrate (angiotensin

I) for active site of ACE; inhibition of ACE initially results in decreased plasma angiotensin II

concentrations and consequently, blood pressure may be reduced in part through decreased

vasoconstriction, increases renin activity, and decreases aldosterone secretion; also increases

renal blood flow, results to afterload reduction.

Until the patency of the ductus is corrected, administer antibiotics in patient during

instances of high exposure to bacteremia is needed. As recommended bye the american heart

association for the prevention of bacterial endocarditis. Ceftriaxone, ampicillin and gentamicin is

antibiotics drugs which used for eliminate and prevention bacterial endocarditis. Ceftriaxon is

Third generation cephalosporin with broad spectrum gram negative activity, has lower efficacy

against gram-positive organisms but higher efficacy against resistant organism, highly stable in

presence of beta lactamase (penicilinase and cephalosporinase) of gram-negative and gram-

positive bacteria. bactericidal activity results from inhibiting cell wall synthesis by binding to 1

or more penicillin binding proteins, exerts antimcrobial effect by interferingwith syhthesis of

peptidoglycan (major structural component of bacterial cell wall). bacteria eventually lyse

because activity of cell wall autolytic enzymes continues while cell wall assembly is arrested.

Ampicilin is Broad spectrum penicillin. Interferes with bacterial cell wall synthesis during active

replication, causing bactericidal activity against susceptible organism.alternative to amoxicilin

when unable to take medication orally.

Gentamycin is Aminoglycoside antibiotic for gram negatif coverage bacteria including

pseudomonas species. Synergistic with beta-lactamse against enterococci. Interferes with

bacterial protein synthesis by binding to 30s and 50s ribosomal subunits.

Conclusion

This paper reports a case of a 11 years old female diagnosed with congestive heart failure et

causamoderate Patent Ductus Arteriosus + vegetation o/t pulmonary valve + mild PE + mild PI +

mild MI + mild TI. A comprehensive work up had been done to confirm the diagnosis. The

treatment for this patient includes Furosemide and Spironolactone for reducing pre-load,

Captopril for reducing after-load, Ampicillin and Gentamicin for bacterial endocarditis

prevention and eradication, ambroxol for cough. O2 and semi fowler position are meant to treat

shortness of breath, and adequat diet for malnutrition.

References

1. Schneider DJ, Moore JW. Patent ductusarteriosus. Circulation 2006;114:1873-1882.

2. Hajjar ME, Vaksmann G, Rakza T, et al. Severity of the ductal shunt: a comparison of

different markers. Arch Dis Child Fetal Neonatal Ed 2005;90:F419-F422.

3. Hammerman C. Patent ductusarteriosus. Clinical relevance of prostaglandins and

prostaglandin inhibitors in PDA pathophysiology and treatment. ClinPerinatol

1995;22:457-479

4. Ellison RC, Peckman GJ, Lang P, et al. Evaluation of the preterm infant for patent

ductusarteriosus. Pediatrics 1983;71:364-372.

5. Pegoli W. Pericardium and great vessels. In: Oldham KT, Colombiani PM, et al., editors.

Principles and Practice of Pediatric Surgery. 4th ed. Philadelphia, PA: Lippincott

Williams & Wilkins; 2005:1019.

6. Smith GC. The pharmacology of the ductusarteriosus. Pharmacol Rev 1998;50:35-58.

7. Miao CY, Zuberbuhler JS, ZuberbuhlerJR. Prevalence of congenital cardiacanomalies at

high altitude. J Am CollCardiol 1990;12:224-228.

8. Nora JJ, Nora AH. Recurrence risksin children having one parent with a congenital heart

disease. Circulation1976;53:701-702.

9. Gittenberger-de Groot AC, Moulaert AJ,Hitchcock JF. Histology of the

persistentductusarteriosus in cases of congenitalrubella. Circulation 1980;62:183-186.

10. Ivey KN, Srivastava D. The paradoxicalpatent ductusarteriosus. J Clin

Invest2006;166:2863-2866.

11. Clyman RI. Ibuprofen and patent ductusarteriosus. New Engl J Med 2000;343:728-739.

12. Hermes-DeSantis ER, Clyman RI. Patent ductusarteriosus: pathophysiology and

management. J Perinatol 2006;26:S14-S18.

13. VanOvermeire B, Chemtob S. The pharmacologic closure of the patent ductusarteriosus.

Semin Fetal Neonatal Med2005;10:177-184.

14. Clyman RI, Campbell D, Heymann MA,et al. Persistent responsiveness of theneonatal

ductusarteriosus in immaturelambs: a possible cause for reopeningof patent

ductusarteriosus after indomethacin-induced closure. Circulation1985;71:141-145.

15. Clyman RI, Mauray F, Rudolph AM, etal. Age dependent sensitivity of the

lambductusarteriosus to indomethacin andprostaglandins. Circulation 1980;93:94-98.

16. Bernard T, Michelakis ED, Wu X, et al. Oxygen-sensitive Kv channel gene transfer

confers oxygen responsiveness to preterm rabbit and remodeled human ductusarteriosus:

implications for infants with patent ductusarteriosus. Circulation 2004;110:1372-1379.

17. Fay FS, Kooke PH. Guinea pig ductusarteriosus, II: irreversible closure after birth. Am J

Physiol. 1972;222:841– 849.

18. Hoffman JIE, Buckberg GD. Regional myocardial ischemia: causes, prediction, and

prevention. Vasc Surg. 1974;8:115–131.

19. Becker TE, Ensing GJ, Darragh RK, Caldwell RL. Doppler derivation ofcomplete

pulmonary artery pressure curves in patent ductusarteriosus.Am J Cardiol. 1996;78:1066

–1069.

20. Morgan-Jughes GJ, Marshall AJ, Roobottome C. Morphologicassessment of patent

ductusarteriosus in adults using retrospectivelyECG-gated multidetector CT. Am J

Roentgenol. 2003;181:749 –754.

21. Brenner LD, Caputo GR, Mostbeck G, Steiman D, Dulce M, CheitlinMD, O’Sullivan M,

Higgins CB. Quantification of left to right atrialshunts with velocity-encoded cine nuclear

magnetic resonance imaging.J Am CollCardiol. 1992;20:1246 –1250.

22. Kussman GD, Geva T, McGowan FX. Cardiovascular causes of airwaycompression.

PediatrAnaesth. 2004;14:60 –74.

23. Taneja K, Gulati M, Jain M, Saxena A, Das B, Rajani M. Ductal arteriosus aneurysm in

the adult: role of computed tomography in diagnosis. ClinRadiol. 1997;52:231–234.

24. Fisher RG, Moodie DS, Sterba R, Gill CC. Patent ductusarteriosus inadults—long term

follow-up: nonsurgical vs surgical treatment. J Am CollCardiol. 1986;8:280 –284.

25. Pas D, Missauld L, Hollanders G, Suys B, DeWolf D. Persistent ductusarteriosus in the

adult: clinical features and experience with percutaneousclosure.

ActaCardiol2002;57:275–278.

26. Rao, PS. Summary and comparison of patent ductusarteriosus closuremethods. In: Rao

PS, Kern MJ, eds. Catheter Based Devices for theTreatment of Non-Coronary

Cardiovascular Disease in Adults andChildren. Philadelphia, Pa: Lippincott Williams &

Wilkins; 2003:219–228.