CHAPTER I

INTRODUCTION

I.1 Background

The estimated incidence of patent ductus arteriosus (PDA) in US children born at term
is between 0.02% and 0.006% of live births. This incidence is increased in children who are
born prematurely (20% in premature infants > 32 weeks' gestation up to 60% in those < 28
weeks' gestation), children with a history of perinatal asphyxia, and, possibly, children born at
high altitude. In addition, up to 30% of low birth weight infants (< 2500 g) develop a patent
ductus arteriosus (PDA). Siblings also have an increased incidence. Perinatal asphyxia usually
only delays the closure of the ductus, and, over time, the ductus typically closes without
specific therapy. As an isolated lesion, patent ductus arteriosus (PDA) represents 5-10% of all
congenital heart lesions. It occurs in approximately 0.008% of live premature births. No data
support a race predilection. However, there is a female preponderance (female-to-male ratio,
2:1) if the patent ductus arteriosus (PDA) is not associated with other risk factors. In patients
in whom the patent ductus arteriosus (PDA) is associated with a specific teratogenic exposure,
such as congenital rubella, the incidence is equal between the sexes. (1)

Among 220 millions peoples in Indonesia, there are 40.000 new cases of congenital
heart disease every year, actually it is only about 2% cases held by clinician, lower than other
developed countries (2). The incidence rate of PDA in preterm infants was 14%. Furthermore,
the lower the birth weight, the higher the incidence rate of PDA and the presence of RDS is
related to the delay in the closing of the arterial duct (3)

The prognosis is generally considered excellent in patients in whom the patent ductus
arteriosus (PDA) is the only problem. In premature infants who have other sequelae of
prematurity, these sequelae tend to dictate prognosis of patent ductus arteriosus (PDA).
Morbidity and mortality rates are directly related to the flow volume through the ductus
arteriosus. A large patent ductus arteriosus (PDA) may cause congestive heart failure (CHF);
if left untreated for a long period, pulmonary hypertension may develop. (1)
Daftar Pustaka Bab 1

1. Patent Ductus Arteriosus. http://emedicine.medscape.com/article/891096-

overview#showall date accessed : May 20, 2013
2. Departemen Kesehatan Republik Indonesia. 2007.
buk.depkes.go.id/index.php?option=com. [date accessed May 20, 2013]
3. Deselina Benita, MD., Putra T. Sukman, MD., Suradi Rulina, MD. 2004.
Prevalence of Patent Ductus Arteriosus in Premature infants at the Neonatal
Ward, Cipto Mangunkusumo Hospital, Jakarta. In: Paediatrica Indonesiana
vol.44. Accessed from: http://www.paediatricaindonesiana.org/?q=a&a=423,
[date accessed May 20, 2013]

1.2 Objectives
This study aim to obtain knowledge and understanding about congenital heart
disease for co-assistant especially in Patent Ductus Arteriosus, preparing as a
good general practitioner as the first line clinician in community.
 CHAPTER II
LITERATURE REVIEW

2.1. Patent Ductus Arteriosus

2.1.1. Definition
The ductus arteriosus is the vessel that connects the left pulmonary artery to the
descending aorta during fetal life. Patent ductus arteriosus ( PDA ) results when the ductus
fails to close after birth, resulting in a persistent connection between the great vessels. 1

2.1.2. Etiology
The factors responsible for persistent patency of the ductus arteriosus beyond the first
24 to 48 hours of neonatal life are not completely understood. Prematurity clearly increases
the incidence of PDA, and this is due to physiological factors related to prematurity rather
than inherent abnormality of the ductus. Several factors are involved, including immaturity of
the smooth muscle within the structure or the inability of the immature lungs to clear the
circulating prostaglandins that remain from gestation. These mechanisms are not fully
understood. Conditions that contribute to low oxygen tension in the blood, such as immature
lungs, coexisting congenital heart defects, and high altitude, are associated with persistent
patency of the ductus. In term infants, cases most often appear to occur sporadically, but there
is increasing evidence that genetic factors play a role in many patients with patent ductus.2

2.1.3. Epidemiology
The persistence of a PDA is much more common in preterm than term infants. This is
secondary to the immaturity of the duct. Since the advent of echocardiography, the incidence
of PDA in children born at term has been reported as approximately 1 to 2 per 1000. This
estimate is higher than previously thought since it includes clinically silent PDAs. This higher
estimate comes with inclusion of clinically silent PDAs. There is globaly higher incidence in
females as well as in children born at higher altitudes.

Embryology
The ductus arteriosus is a normal and essential fetal structure that becomes abnormal if
it remains patent after the neonatal period. In normal cardiovascular development, the
proximal portions of the sixth pair of embryonic aortic arches persist as the proximal branch
pulmonary arteries, and the distal portion of the left sixth arch persists as the ductus
arteriosus,connecting the left pulmonary artery with the left dorsal aorta. Normally, the distal
right sixth aortic arch loses its connection to the dorsal aorta and degenerates. This
transformation is complete by 8 weeks of fetal life.3

Normal Physiology
Fetal Circulation
Whereas 65% of the fetal cardiac output is from the right ventricle, only 5% to 10%
passes through the lungs.The preponderance of right ventricular output passes through the
ductus arteriosus into the descending aorta. The fetal ductus arteriosus is thus an important
structure that is essential for normal fetal development, permitting right ventricular output to
be diverted away from the high-resistance pulmonary circulation. Premature constriction or
closure may lead to right heart failure, resulting in fetal hydrops.2,3

Mechanisms of Normal Closure

Grossly, the constitution of the fetal ductus arteriosus appears to be similar to the
contiguous main pulmonary artery and descending aorta; After birth, the abrupt increase in
oxygen tension inhibits ductal smooth muscle voltage-dependent potassium channels,which
results in an influx of calcium and ductal constriction. The medial smooth muscle fibers in the
ductus contract, which results in wall thickening, lumen obliteration, and shortening of the
ductus arteriosus. 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.2,3

Anatomy
In the normal heart with a left-sided aortic arch, the ductus arteriosus connects the left
pulmonary artery near its origin to the descending aorta just distal to the left subclavian artery.
The ductus arteriosus may persist in a wide variety of sizes and configurations. Usually, the
aortic end of the patent ductus is larger than the pulmonary artery end, which results in a
somewhat conical configuration. The size, configuration, and relationship to adjacent
structures are important with respect to determining resistance to blood flow (an important
determinant in the degree of shunting) and also have important implications with regard to
interventional closure.2,3
Figure 1. Schematic of embryonic aortic arch system. The 6 pairs of embryonic aortic arches
are demonstrated (left-sided arches are numbered). The portions that normally involute are
indicated by broken lines. The distal left sixth embryonic arch normally persists and becomes
the PDA, connecting the left pulmonary artery to the proximal descending aorta.

2.1.4. Patophysiology

As described earlier, the smooth muscle of the ductus arteriosus usually constricts
after birth owing to the sudden rise in blood oxygen tension and a reduction in the level of
circulating prostaglandins. Over the next several week, intimal proliferation and fibrosis result
in permanent closure. Failure of the ductus to close results in a persistent shunt between the
descending aorta and the left pulmonary artery. The magnitude of low through the shunt
depends on the cross-sectional area and lenght of the ductus itself as well as the relative
resistents of the systemic and pulmonary vasculatures. Prenatally, when the pulmonary
vascular resistent is high, blood is diverted away from the immature lung to the aorta. As the
pulmonary resistance drops postnatally, the shunt reverses direction and blood flows from the
aorta into the pulmonary circulation instead. Because of this left-to-right shunt, the pulmonary
circulation, left artrium, and LV become volume overloaded. This can lead to left ventricular
dilatation and left sided heart failure, whereas the right heart remains normal unless
pulmonary vascular disease ensues. If the latter does develop, eissenmenger syndrome result,
with reversal of the shunt causing blood to flow fom the pulmonary artery, through the ductus,
to the descending aorta.the resulting flow of the saturated blood to the lower extremitis causes
cyanosis of the feet; the upper extremitis are not cyanotic, because they receive normally
saturated blood from the proximal aorta.1

Symptom and Sign

The clinical findings and the clinical course depend on the size of the shunt and the degree of
pulmonary hypertension.
1. Typical patent ductus arteriosus
The pulses are bounding and pulse pressure is widened. S1 is normal. S2 is usually
narrowly split and very rarely (when the shunt is maximal) paradoxically split (ie, S2 closes
on inspiration and splits on expiration). The paradoxic splitting is caused by the volume
overload of the left ventricle and the prolonged ejection of blood from this chamber. The
murmur is quite characteristic. It is a very rough machinery murmur that is maximal at the
second intercostal space at the left sternal border and inferior to the left clavicle. It begins
shortly after S1, rises to a peak at S2, and passes through the S2 into diastole, where it
becomes a decrescendo murmur and fades before the S1. The murmur tends to radiate fairly
well over the lung fields anteriorly but relatively poorly over the lung fields posteriorly. A
diastolic flow murmur is often heard at the apex.5
2. Patent ductus arteriosus with pulmonary hypertension
The physical findings depend on the cause of the pulmonary hypertension. If pulmonary
hypertension is primarily the result of a marked increase in blood flow and only a slight
increase in pulmonary vascular resistance, the physical findings are similar to those listed
above. The significant difference is the presence of an accentuated pulmonary component of
S2. Bounding pulses and a loud continuous heart murmur are present. In patients with
increased pulmonary vascular resistance, the findings are quite different. S2 is single and
quite accentuated, and there is no significant heart murmur. The pulses are normal rather than
bounding.5
3. Patent ductus arteriosus in the premature neonate with associated respiratory
distress syndrome
A preterm neonate during or after the respiratory distress syndrome may have a
significant PDA that is difficult to detect by auscultation but that is often clinically significant.
A soft, nonspecific systolic murmur or no murmur is heard rather than the classic continuous
murmur. The peripheral pulses may be increased, which is a helpful sign. An early sign
indicating the presence of a significant left-to-right shunt with concomitant congestive heart
failure is increasing dependence on oxygen and respiratory support. In addition, the chest x-
ray may show cardiomegaly. In any case, echocardiography must be performed to determine
the presence or absence of a PDA in the premature infant with lung disease.5

Clinical findings and associations

Patent ductus arteriosus is associated with several neonatal morbidities. Both animal
and human studies have demonstrated alterations in blood pressure with a drop in the mean,
as well as, systolic and diastolic pressures. Left ventricular output can increase by as much as
100%. In spite of this increased cardiac output, redistribution in blood flow results in
increased flow to the lungs and decreased flow to the pressure passive organs like the
intestines, skin, muscle, and kidneys. This redistribution may result in metabolic acidosis,
necrotizing enterocolitis (NEC), and pulmonary edema/hemorrhage. Timing is important in
evaluating when different morbidities will present. Intracranial hemorrhage usually occurs
within the first 3 days after birth. Similarly, marked pulmonary edema and pulmonary
hemorrhage secondary to fluid shifts and ductus patency occurs within 23 days after birth.
Necrotizing enterocolitis usually presents 5 days after birth.3,5,6

2.1.5. Diagnosis and Work Up1,2,3

a) History taking
Premature
Genetics
b) Clinical Features

Bigger PDA will automatically make blood volume become much more to the lungs. On
a baby or child with PDA will show some symptoms :

Unthirsty
No increase in weight
Sweating a lot
Hard to breath
Tachicardia
fatigue
lack of growth

The symptoms shows that a congestive heart failure had. Meanwhile if the PDA is
small, risk of congestive heart failure is very small, only need to be alert on a risk of
endocarditis. Endokarditis can be fatal if there is no treatment that how it should be.

On physical examination will show some sign :

Takhipnoe
Takikardi
sweating
cyanotic
water hammer pulse is the unique sign, this can be happened because of the leak
of blood from the aorta in systole or diastole, so a big pulse pressure will be found.

Palpation :

Thrill sistolik clearly palpable on left ICS II that can spread around.
incfrease of pulomonary artery pressure, heart sound II become louder so
will be palpable on ICS II at left of sternum.

Auscultation :

First sound of the heart usually normal, followed by click sistolic.

Second sound of the heart always louder, loudest heard at left ICS II.
 Punctum Machinery murmur maximum at left sternal ICS II. Noisy sound
in the systole periode heard crescend and ended on second heart sound
otherwise noisy sound in the diastole period heard decrescend, heard best
in a supine position, place and the sounds intencity arent related with the
respiration.
On a patient with a large PDA, there will be a mid-diastolic murmur on a
mitral presentation that will be heard at the apeks as a result of a increasing
of a blood volume through the mitral.

IMAGING
In simple PDA, the x-ray appearance depends on the size of the shunt. If the shunt is
relatively small, the heart is not enlarged. If the shunt is large, evidence indicates both left
atrial and left ventricular enlargement. In both cases, the aorta is prominent, as is the main
pulmonary artery segment.4,6

ELECTROCARDIOGRAPHY
The ECG may be normal or may show left ventricular hypertrophy, depending on the
size of the shunt. In patients with pulmonary hypertension caused by increased blood flow,
biventricular hypertrophy usually occurs. In those with pulmonary vascular obstructive
disease, pure right ventricular hypertrophy occurs.6

ECHOCARDIOGRAPHY
The two-dimensional echocardiography shows left atrial and ventricular enlargement,
but imaging of the ducts itself is usually difficult in adult. The use of color flow, pulsed
Doppler ultrasonography, and two-dimensional echocardiography provides direct
visualization of the ductus and confirmation of the direction and degree of shunting. Preterm
infants with a suspected PDA should have a complete echocardiographic evaluation to make a
definitive diagnosis, assess the magnitude of the left-to-right shunt, and to rule out associated,
particularly ductus-dependent, lesions. Pulmonary artery pulse can be estimated from the
almost ubiwuitous tricuspid regurgitant jet.4,6

CARDIAC CATHETERIZATION AND ANGIOCARDIOGRAPHY

 Children with PDA never require a cardiac catheterization for diagnostic reasons.
However, children with a small PDA routinely have the duct closed in the catheterization
laboratory. This is the sole indication for cardiac catheterization in PDA. Techniques for coil
and, more recently, device occlusion are well established and currently represent the treatment
of choice for simple PDAs in many institutions. Thus, catheterization should be combined
with therapeutic intervention. Selective angyographi is a tools to locate and see how big the
duct. Angyiography also used to explain the anatomy of intracardiac when there is another
problem inside the heart to be proved.4,6

Treatment
Treatment consists of surgical correction when the PDA is large, except in patients
with pulmonary vascular obstructive disease. Patients with large left-to-right shunts and
pulmonary hypertension should be operated on by age 1 year to prevent the development of
progressive pulmonary vascular obstructive disease. Simple PDA should be corrected after
the child reaches age 6 months, although the operation may be delayed until later without
increasing the risk of death.

Medicamentosa
Symptomatic PDA is a frequent problem in preterm infants. Indomethacin, a potent
inhibitor of prostaglandin synthesis, is routinely used to try to close the PDA in premature
infants. Indomethacin does not close the PDA of term infants or children. The success of
indomethacin therapy is as high as 8090% in premature infants over 1200 g birth weight, but
it is less successful in smaller infants. Indomethacin (0.10.3 mg/kg orally every 824 hours
or 0.10.3 mg/kg parenterally every 12 hours) can be used only if adequate renal,
hematologic, and hepatic function is demonstrated. Management during indomethacin therapy
includes fluid restriction with or without diuretics and close observation of the urinary output
because indomethacin can rapidly decrease renal function.7,6,8
Repeat echocardiography is used to monitor the effectiveness of the indomethacin
therapy. If indomethacin is not successful and the ductus remains hemodynamically
significant, then surgical ligation should be performed without hesitation. If the ductus closes
substantially so that it is not longer hemodynamically significant but there is still some flow
through it from left to right, surgery is not needed and a second course of indomethacin may
complete ductal closure. Recent studies from Europe indicate that ibuprofen may be as
effective as indomethacin for the medical closure of the preterm PDA.7,6,8
Tabel 1 Contraindications to the administration of indomethacin 6
Active bleeding
Active or suspected necrotizing enterocolitis
Creatinine X2.0 mg/dl
Urine output <0.6 ml/kg/h
Platelet count <50 000
Active and untreated infection
Suspected congenital heart disease
Known gastrointestinal or renal anomaly

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.
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. 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 thoracotomy and by the technique of
video-assisted thoracoscopic ligation of the PDA.1,3,6,7

Surgery indication on PDA:

1. PDA on a baby that no respond on the medicamentosa therapy.
2. PDA with symtomps.
3. PDA with infective endocarditis that do not respond the medicamentosa.

Transcatheter Closure
Transcatheter occlusion has become the treatment of choice for most patent ductus in
children and adults. In cases of calcified ductus arteriosus 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.
 Transcatheter closure of small defects with one or more Dacron-coated coils has
become standard therapy. Patients with nonreactive pulmonary vascular obstruction who have
resistance greater than 10 units and a ratio of pulmonary to systemic resistance greater than
0.7 despite vasodilator therapy (eg, nitric oxide) should not be operated on. These patients are
made worse by closure of the ductus, because the ductus serves as an escape route for their
pulmonary hypertension.

Complication
Infective endarteritis may be seen at any age. Pulmonary or systemic emboli may
occur. Rare complications include aneurysmal dilatation of the pulmonary artery or the
ductus, calcification of the ductus, noninfective thrombosis of the ductus with embolization,
and paradoxical emboli. Pulmonary hypertension (Eisenmenger syndrome) usually develops
in patients with a large PDA who do not undergo surgical treatment.1,2,4,7

Course & Prognosis

Patients with simple PDA and small to moderate shunts usually do quite well even
without surgery. However, in the third or fourth decade of life, symptoms of easy fatigability,
dyspnea on exertion, and exercise intolerance appear, usually as a consequence of the
development of pulmonary hypertension or congestive heart failure.
Spontaneous closure of a PDA may occur up to age 1 year. This is especially true in
infants who were born preterm. After age 1 year, spontaneous closure is rare. Because
infective endocarditis is a potential complication, closure by coil embolization or surgery is
recommended if the defect persists beyond age 1 year.
Patients with large shunts or pulmonary hypertension do not do as well. Poor growth
and development, frequent episodes of pneumonia, and the development of congestive heart
failure occur in these children. Therefore, patients with PDA and large shunts who are beyond
the newborn period should have immediate surgical ligation of their PDA.
 BAB III

CASE REPORT

History of Present Disease

A 5 month old boy (MSP/ MR 55 86 73) was admitted at May 9th, 2013 to hospitalization
Haji Adam Malik with chief complained history shortness of breath since three months and
getting worse for the last one and half months. The shortness of breath is not related to the
weather, but it getting worse by the activity. Dyspnea usually occur after he cried or sneezing
and blue appearance showed but it disappear immediately. History of discontinuity while
suckle found. History sweating while suckle was not found. History of fever, loss of appetite,
and weight loss was not found. Those patient come to RSUP HAM as a referral from the
Sufina Azis Hospital and already diagnosed as a Moderate PDA with good LV function
examined by echocardiography and planned to get Transcatheter PDA Closure.

He was born in hospital through caesarean section assisted by obstetrician and gynaecologist,
birth body weight was 3000 gram and the birth body length was 46 cm but the APGAR score
was not remembered by her mother. Mothers age 39 years old and history of previous
hypertension was found.

History of Development

- Following object direction : 1 month

- Smile : 2 months
- Laughing : 3 months
- Head lifting : 4 months
- Turning away : 4 months

History of Feeding

- Breast feeding : was given from birth until now

-
History of Immunization
- BCG : 2 month
- DPT : 2, 4 months
- Polio : 0, 2, 4 months
- HBV : 0, 1 months
History of previous illness : unclear
History of previous medications : unclear

Physical Examination
Generalized status
Body weight: 6,3 kg, Body length: 59 cm,
Upper arm circumference: 12 cm, Head circumference: 40 cm
BW/BL : 2<Z<1
BW/age : -2 < Z < 0
BL/age : -3 < Z < -2

Presens status
Consciousness: Alert Heart Rate: 104 x/i
Body temperature: 36,2C Respiratory Rate: 32x/i
General condition was moderate and nutrition condition was good.

Anemic (-). Icteric (-). Cyanosis (-). Edema (-). Dyspnea (-).

Localized status
Head :
Inferior palpebra conjunctiva pale (-/-). Icteric sclera (-). Light reflex (+/+). Isochoric pupil.
Corneal ulcer (-). Bitots spot (-). Ear, nose. mouth were within normal limit.

Neck :
Lymph node enlargement (-). JVP R-2 cmH2O.

Thorax:
Symmetrical fusiformis. Chest retraction (-). HR: 104 bpm, reguler, grade III/VI ICR II/III
LMCS continous murmur (+). RR: 32x/i, reguler. Breath sound: vesicular. Rales (-/-).

Abdomen:
Soepel, peristaltic (+) N, Hepar/Lien: not palpable

Extremities:
Upper extremities Pols: 104 x/i, regular, adequate pressure/volume, CRT < 3, warm, Lower
extremities: oedem (-/-)

Urogenital:
Male, within normal limit

Chest X-Ray on RS Sufina Azis (May 6th 2013)

Echocardiography Result (May 7th 2013) :

Moderate PDA + Left sided enlargement with Good LV Function

Differential Diagnosis:
Moderate PDA + Left sided enlargement with Good LV Function
Working Diagnosis:
Moderate PDA + Left sided enlargement with Good LV Function
Management:
Furosemid 2 x 6 mg
Aldacton 2 x 6,25 mg

Diagnostic Planning:
Transcatheter PDA closure
Follow up on May 9th-10th 2013
May 9th 2013
S Shortness of breath (+)
O Sensorium: compos mentis
Temperature: 37.2C
BW: 6.3 kg
BL: 59 cm
Head : Eyes : Light reflexes : +/+,
isocoric, conjunctiva
palpebra was not pale
Ear, and mouth : normal
Nose : nasal canule
Neck : lymph node was not
palpable
Chest : Simmetrical fusiformis, no
retraction
HR : 100 bpm, reguler,
grade III/VI ICR II/III
LMCS continous murmur
(+)
RR : 30 breathes/minute,
reguler, no rales
Abdomen : Soepel, peristaltic (+)
normal, liver and spleen
unpalpable
Extremities : pulse 100 bpm, reguler,
pressure and volume were
adequate, warm acral,
CRT <3
A Working Diagnosis : Working Diagnosis :
Moderate PDA + Left sided enlargement Moderate PDA + Left sided enlargement
with Good LV Function
P O2 L/I nasal canule
Furosemide 2 x 6 mg
Aldactone 2 x 6.25 mg
Nebule / 6 hr with NaCl 0.9% 2.5 cc
R/ Transcatheter PDA closure
May 10th 2013
Shortness of breath (+)
Sensorium: compos mentis
Temperature: 36.7C
BW: 6.3 kg
BL: 59 cm
Head : Eyes : Light reflexes : +/+,
isocoric, conjunctiva palpebra
was not pale
Ear and mouth : normal
Nose : nasal canule fixed
Neck : lymph node was not palpable
Chest : Simmetrical fusiformis, no
retraction
HR : 98 bpm, reguler, grade
III/VI ICR II/III LMCS
continous murmur (+)
RR : 26 breathes/minute,
reguler, no rales
Abdomen : Soepel, peristaltic (+) normal,
liver and spleen unpalpable
Extremities : pulse 98 bpm, reguler,
pressure and volume were
adequate, warm acral, CRT
<3.
with Good LV Function
O2 L/I nasal canule
Furosemide 2 x 6 mg
Aldactone 2 x 6.25 mg
Nebule / 6 hr with NaCl 0.9% 2.5 cc
Diet MII 630 kkal + 12 gr protein
R/ Transcatheter PDA closure
Laboratory result : May 10th 2013

Parameters Value Normal Value

Complete Blood Count
Hemoglobin 10,60 gr% (10,7 17,1) gr%
Erithrocyte 4.84 x 106 /mm3 (3.75-4.95) x 106 /mm3
Leucocyte 13.35 x 103 /mm3 (6.0-17.5) x 103 /mm3
Hematocrite 33.10 % (38-52) %
Trombocyte 649 x 103 /mm3 (217-497) x 103 /mm3
MCV 68.40 fL (93-115) fL
MCH 21.90 pg (29-35) pg
MCHC 32.00 g% (28-34) %
RDW 14.90 % (14.9-18.7) %
MPV 7.90 fL (7.2-10.0) fL
PCT 0.51%
PDW 8.3 fL
Diftel
Neutrofil 20.70 % (37-80) %
Limfosit 64.90 % (20-40) %
Monosit 10.90 % (2-8) %
Eosinofil 3.10 % (1-6) %
Basofil 0.400 % (0-1) %
Neutrofil absolute 2.76 x 103/L (1.9-5.4) x 103/L
Limfosit absolute 8.66 x 103/L (3.7-10.7) x 103/L
Monosit absolute 1.46 x 103/L (0.3-0.8) x 103/L
Eosinofil absolute 0.42 x 103/L (0.20-0.50) x 103/L
Basofil absolute 0.05 x 103/L (0-0.1) x 103/L
Faal Hemostatic
Bleeding Time 3.30 minute < 5 minute
PT + INR
Protrombine Time
Control 13.20 sec
Patient 15.6 sec
INR 1.20
APTT
Control 29.9 sec
Patient 39.6 sec
Trombine time
Control 13.2 sec
Patient 13.4 sec
Clinic Chemistry
Hepar
Total bilirubin 0.39 mg/dL <1
Direct bilirubin 0.33 mg/dL 0 0.2
Fosfatase alkali (ALP) 338 U/L < 449 U/L
AST/SGOT 45 U/L < 38 U/L
ALT/SGPT 17 U/L < 41
Carbohydrate Metabolism
Blood glucose (at the 106.00 mg/dL < 200 mg/dL
time)
Renal
Ureum 26.40 mg/dL < 50 mg/dL
Creatinine 0.37 mg/dL 0.17-0.42 mg/dL
Uric acid 5.1 mg/dL < 7.0 mg/dL
Electrolyte
Natrium (Na) 132 mEq/L (135-155) mEq/L
Kalium (K) 4.9 mEq/L (3.6-5.5) mEq/L
Phospor 6.3 mEq/L (5.0-10.8) mEq/L
Chlor (Cl) 96 mEq/L (96-106) mEq/L
Magnesium (Mg) 2.58 mEq/L (1.4-1.9) mEq/L
Immunoserology
Hepatitis
HBsAg Negative Negative
Hepatitis A Profile
Anti HAV Total 60.00 Negative
(Negative < 20 Positive >= 20)
Hepatitis C
Anti HCV Negative
May 11st 2013
S Shortness of breath (+)
O Sensorium: compos mentis
Temperature: 37C
BW: 6.3 kg
BL: 59 cm
Head : Eyes : Light reflexes : +/+,
isocoric, conjunctiva
palpebra was not pale
Ear and mouth : normal
Nose : nasal canule fixed
Neck : lymph node was not
palpable
Chest : Simmetrical fusiformis,
retraction (+) in
epigastrial
HR : 100 bpm, reguler,
grade III/VI ICR II/III
LMCS continous murmur
(+)
RR : 25 breathes/minute,
reguler, no rales
Abdomen : Soepel, peristaltic (+)
normal, liver and spleen
unpalpable
Extremities : pulse 100 bpm, reguler,
pressure and volume were
adequate, warm acral,
CRT <3
A Working Diagnosis : Working Diagnosis :
Moderate PDA + Left sided enlargement Moderate PDA + Left sided enlargement
with Good LV Function
P O2 L/I nasal canule
Furosemide 2 x 6 mg
Aldactone 2 x 6.25 mg
Nebule / 8 hr with NaCl 0.9% 2.5 cc
Diet MII 630 kkal + 12 gr protein
R/ Transcatheter PDA closure
Negative
May 12th 2013
Shortness of breath (-)
Sensorium: compos mentis
Temperature: 37C
BW: 6.2 kg
BL: 59 cm
Head : Eyes : Light reflexes : +/+,
isocoric, conjunctiva palpebra
was not pale
Ear and mouth : normal
Nose : nasal canule fixed
Neck : lymph node was not palpable
Chest : Simmetrical fusiformis,
retraction (+) epigastrial
HR : 90 bpm, reguler, grade
III/VI ICR II/III LMCS
continous murmur (+)
RR : 40 breathes/minute,
reguler, no rales
Abdomen : Soepel, peristaltic (+) normal,
liver and spleen unpalpable
Extremities : pulse 90 bpm, reguler,
pressure and volume were
adequate, warm acral, CRT
<3.
with Good LV Function
O2 L/I nasal canule
Furosemide 2 x 6 mg
Aldactone 2 x 6.25 mg
Nebule / 8 hr with NaCl 0.9% 2.5 cc
Diet MII 630 kkal + 12 gr protein
R/ Transcatheter PDA closure
 May 13th 2013
S Shortness of breath (-)
O Sensorium: compos mentis
Temperature: 37C
BW: 6.2 kg
BL: 59 cm
Head : Eyes : Light reflexes : +/+,
isocoric, conjunctiva
palpebra was not pale
Ear and mouth : normal
Nose : nasal canule fixed
Neck : lymph node was not
palpable
Chest : Simmetrical fusiformis,
retraction (+) in
epigastrial
HR : 100 bpm, reguler,
grade III/VI ICR II/III
LMCS continous murmur
(+)
RR : 38 breathes/minute,
reguler, no rales
Abdomen : Soepel, peristaltic (+)
normal, liver and spleen
unpalpable
Extremities : pulse 100 bpm, reguler,
pressure and volume were
adequate, warm acral,
CRT <3
A Working Diagnosis : Working Diagnosis :
Moderate PDA + Left sided enlargement Moderate PDA + Left sided enlargement
with Good LV Function
P O2 L/I nasal canule
Furosemide 2 x 6 mg
Aldactone 2 x 6.25 mg
Nebule / 8 hr with NaCl 0.9% 2.5 cc
Diet MII 630 kkal + 12 gr protein
R/ Transcatheter PDA closure
May 14th 2013
Shortness of breath (+)
Sensorium: compos mentis
Temperature: 36.8C
BW: 6.2 kg
BL: 59 cm
Head : Eyes : Light reflexes : +/+,
isocoric, conjunctiva palpebra
was not pale
Ear and mouth : normal
Nose : nasal canule fixed
Neck : lymph node was not palpable
Chest : Simmetrical fusiformis,
retraction (+) epigastrial
HR : 108 bpm, reguler, grade
III/VI ICR II/III LMCS
continous murmur (+)
RR : 30 breathes/minute,
reguler, no rales
Abdomen : Soepel, peristaltic (+) normal,
liver and spleen unpalpable
Extremities : pulse 108 bpm, reguler,
pressure and volume were
adequate, warm acral, CRT
<3.
with Good LV Function
O2 L/I nasal canule
Furosemide 2 x 6 mg
Spinorolactone 2 x 6.25 mg
Nebule / 8 hr with NaCl 0.9% 2.5 cc
Diet MII 630 kkal + 12 gr protein
R/ Transcatheter PDA closure
 May 15th 2013 May 15th 2013 (follow up post trancatheter
closure)
S Shortness of breath (-) Bleeding (-)
O Sensorium: compos mentis Sensorium: compos mentis
Temperature: 37.1C Temperature: 36.9C
BW: 6.2 kg BW: 6.2 kg
BL: 59 cm BL: 59 cm

Head : Eyes : Light reflexes : +/+, Head : Eyes : Light reflexes : +/+,
isocoric, conjunctiva isocoric, conjunctiva palpebra
palpebra was not pale was not pale
Ear and mouth : normal Ear and mouth : normal
Nose : nasal canule fixed Nose : nasal canule fixed
Neck : lymph node was not Neck : lymph node was not palpable
palpable Chest : Simmetrical fusiformis,
Chest : Simmetrical fusiformis, retraction (+) epigastrial
retraction (+) in HR : 128 bpm, reguler,
epigastrial murmur (-)
HR : 110 bpm, reguler, RR : 30 breathes/minute,
grade III/VI ICR II/III reguler, no rales
LMCS continous murmur Abdomen : Soepel, peristaltic (+) normal,
(+) liver and spleen unpalpable
RR : 36 breathes/minute, Extremities : pulse 128 bpm, reguler,
reguler, no rales pressure and volume were
Abdomen : Soepel, peristaltic (+) adequate, warm acral, CRT
normal, liver and spleen <3.
unpalpable
Extremities : pulse 110 bpm, reguler,
pressure and volume were
adequate, warm acral,
CRT <3

A Working Diagnosis : Working Diagnosis :

Moderate PDA + Left sided enlargement Post transcatheter PDA closure (H-1)
with Good LV Function

P O2 L/I nasal canule Inj Ceftriaxone 300 mg/12 hr/IV (2x)

Furosemide 2 x 6 mg Diet MB 620 kkal + 12 gr protein
Spironolactone 2 x 6.25 mg
Nebule / 8 hr with NaCl 0.9% 2.5 cc
Diet MII 630 kkal + 12 gr protein
R/ Transcatheter PDA closure
(15/5/2013)
Cath and Transcatheter PDA Closure (May 15th 2013)

Conclusion : Succesful Transcatheter PDA Closure with Heart 4/6

No residual PDA and no Coarctation

Advice : Keep NBM till fully aware

Guidance IV ceftriaxone 250 mg 2x

Watch bleeding at puncture site and pulsation

Plan for tomorrow : Chest X-Ray (AP and lateral) and Echocardiography
 May 16th 2013 May 17th 2013
S Shortness of breath (-), fever (-), Cough (+) Cold (-), Fever (-)
weakness (+)
O Sensorium: compos mentis Sensorium: compos mentis
Temperature: 36.7C Temperature: 36.8C
BW: 6.2 kg BW: 6.2 kg
BL: 59 cm BL: 59 cm

Head : Eyes : Light reflexes : +/+, Head : Eyes : Light reflexes : +/+,
isocoric, conjunctiva isocoric, conjunctiva palpebra
palpebra was pale (+/+) was pale (+/+)
Ear, nose, and mouth : Ear, nose, and mouth : normal
normal
Neck : lymph node was not Neck : lymph node was not palpable
palpable Chest : Simmetrical fusiformis,
Chest : Simmetrical fusiformis, retraction (+) epigastrial
retraction (+) in HR : 96 bpm, reguler, grade
epigastrial murmur (-)
HR : 100 bpm, reguler, RR : 30 breathes/minute,
murmur (-) reguler, no rales
RR : 36 breathes/minute, Abdomen : Soepel, peristaltic (+) normal,
reguler, no rales liver and spleen unpalpable
Abdomen : Soepel, peristaltic (+) Extremities : pulse 96 bpm, reguler,
normal, liver and spleen pressure and volume were
unpalpable adequate, warm acral, CRT
Extremities : pulse 100 bpm, reguler, <3.
pressure and volume were
adequate, warm acral,
CRT <3

A Working Diagnosis : Working Diagnosis :

Post Transcatheter PDA Closure Post Transcatheter PDA Closure

P Inj. Ceftriaxone 300 mg/12 hr/IV (H1) Inj. Ceftriaxone 300 mg/12 hr/IV (H1)
Diet MB 620 kkal + 12 gr protein Diet MB 620 kkal

R/ Echocardiography R/ Chest X-Ray PA

Chest X-Ray PA Patient may came home and have to
control on schedule
Echocardiography 1 week later

Echocardiography (May 16th 2013) Device in situ, no residual PDA

No LPA stenosis

No coarctation
 Chest X-Ray (May 17th 2013)

Chest X-Ray (May 17th 2013) Bronchopneumonia dextra

Dilatation aorta

CTR 53.06%
 BAB IV
DISCUSSION AND SUMMARY

4.1 Discussion

Patent ductus Arteriosus (PDA) majority From history taking, Baby M was born aterm,
found in preterm baby, low weight baby at deliver through sectio caesarea, his mother
birth, previous history rubela infection in has hypertension with max systolic BP 200
mother, previous history respiratory distress mmHg, his weight at birth doesnt at low
syndrome, history born on high altitude value, history of respiratory distress didnt
know because APGAR SCORE was not
remembered by her mother
PDA show some clinical manifestation like Shortness of breath . The shortness of breath
shortness of breath, tachycardia, tachypnea, is not related to the weather, but it getting
sweating a lot, no increase in weight, fatigue, worse by the activity. History of discontinuity
lack of growth while suckle found. History sweating while
suckle was not found. History lack of growth
was not found.
From physical examination, auscultation may From auscultation, there is grade III/VI ICR
heard continous murmur, mid-diastolic II/III LMCS continous murmur
murmur at the apeks, Punctum Machinery
murmur maximum at left sternal ICS II
Chest X-Ray may normal appearance depend Chest X-Ray not showing cardiomegaly,
on the size of shunt, if the shunt is large, CTR 58.4%
evidence indicates both left atrial and left
ventricular enlargement
Echocardiography result depend on size of Result of echocardiography examination
PDA show moderate PDA and left sided
enlargement with good LV function
Management by medikamentosa, trans Baby M already get trans catheter PDA
catheter PDA closure, open surgery closure
 4.2 Summary

This paper reports a case of a 5-month-old male as a referral from Sufina Azis
Hospital and diagnosed with moderate PDA + left sided enlargement. A comprehensive
treatment including Furosemid, Aldactone, and Spironolactone, and trans catheter PDA
closure has been administered to this patient. He has been stabilized for two days and has
been home and come again on May 24th to control in poly Cardiology.