Asa Pre Board Ent Fix

Patient Case Report
I. Identity
Name : MZ
Gender : Male
Age : 1 years 8 months
Date of Birth : 25 th January 2016
Place of Birth : Pakam
Medical Record : 41.xx.xx
Address : City X
II. History
1. History of Present Illness
Chief complaint: easily tired
Patient complained easily tired since 3 months ago. According to
parents information, patient got tired when running with his friends. No
shortness of breath was complained. Patient experienced recurrent
shortness of breath since he was 1.5 months old, and relapsed every
month for the past 3 months. One month before admission patient was
hospitalized due to shortness of breath for 5 days before reffered to A
hospital. Patient was not cough, patient experienced recurrent chronic
cough since three months old, it usually accompanied with shortness
of breath. Close contact to adult with tuberculosis was denied. Patient
was not cyanotic. History of interrupted feeding and sweating during
feeding were found since birth. No fever and vomit were found,
defecation and urination were normal. Weight gain was difficult to
achieved since 6 months old. His highest achieved body weight was
9.7 kgs in January 2018.
2. History of Past Illness
Patient complained recurrent shortness of breath since he was 1.5
months old and recurrent cough since 3 months old. When patient was
Pre Board National Evaluation, Abdullah Shiddiq Adam, 18th April 2018 1
1.5 months old, parents took him to pediatric cardiologist and
diagnosed with ventricular septal defect according to
echocardiography. Patient routinely checked-up every month and
done echocardiography every 6 months. He took furosemide and
spironolactone. He was advised to undergo defect closure when he
reached 10 kgs.
3. History of Family Illness
History of heart disease in the family was denied. Father was healthy,
37 years of age, and 165 cm of height. Mother was healthy, 32 years
of age, and 158 cm of height. There was no relation between father
and mother.
4. Personal/Social History
a. Antenatal history
Mother routinely visited to midwife and doctor since the 1st month of
pregnancy with 6 visits in total. She took vitamins and iron
supplementation. During pregnancy there was no complaint of
vomiting, bleeding, hypertension or infectious illness. She was not
smoking cigarette, not consuming traditional jamu and also not
drinking alcohol.
b. Natal history
The patient was born preterm with gestasional age 35 week by
spontaneous. The baby cried loudly, active tone, and no cyanosis
immediately after birth. Birth weight and birth lenght were 2600 gram,
49 cm, Mother forgot head circumference.
c. Post natal history
The patient had been recurrent shortness of breath since 1,5 months
of age. There was no history seizure, pale yellowish in this patient.
Conclusion: there is history of infection upper respiratory tract
d. Feeding history
- 0 – 3 months: breast feeding
- 3 – 6 months: Formula milk
- 7 months – 1 year: Formula milk + soft porridge
- 1 year – Now: Formula milk + family meal
Conclusion: Poor of feeding history
e. Developmental history
Growth
According to the mother, Patient had lost 2 kg of weight since this 2
month. Patients had 8.8 kg of weight and 83 cm of height when
hospitalized. Father’s height was 165 cm and mother’s height was 158
cm with genetic potential of height was 159.5 to 176.5 cm.
Development
According to the mother there was no difference between the patient
and her peers. Patient could play and move with her peers.
Conclusion: Abnormal growth and developmental good condition
f. Immunization history
The patient had been taken to primary health care to be vaccinated,
but had not complete yet. Only BCG, hepatitis 0 and polio-1
Conclusion : poor immunization status
g. History of need fulfillment
Biological needs:
Patients did not get exclusive breastfeeding but she received sufficient
clothing, comfortable housing, and access to health care for her
illness.
Affection needs:
The patient is the second child in the family. The oldest sister is 5
years old . The patient received sufficient affection from her parents
and other family members.
Stimulation needs:
The patient received sufficient stimulation from his mother because
since she got ill, the mother took her care by herself at home.
h. Social, economy, and enviroment
Father and mother got married in 2010. Father is 37 years old,
graduated from Senior high school. He works as construction workers.
Mother is 32 years old, graduated from Senior high school, and
she is a housewife. Their monthly income is Rp 2.000.000 until
Rp.2.500.000. Healthcare expenses are covered by national
insurance.. The house has 3 bedrooms, stone wall, concrete floor and
roof. There are many windows and ventilations with adequate lighting.
Water is provided by local water company.
Conclusion: Low social economy family
The condition before observation

( 5th April – 7th April 2018)
Patient came to pediatric cardiology clinic A hospital in 5th April 2018 with
easily tired and hardly achieved weight gain. No shortness of breath and
cough were complained. The patient previously had already been
diagnosed with congenital heart disease with ventricular septal defect
based on echocardiography examination. Echocardiography examination
in 12th February 2018 showed small VSD DCSA (Doubly committed
subarterial) (3-3.2mm), normal pulmonary venous drainage, intact
interatrial septum, mildly dilated Left atrium (LA)-left ventricle (LV), good
LV systolic function.
In 6th April 2018, patient were hospitalized in A hospital. Patient
complained easily got tired. No cough, fever, and shortness of breath were
found. He was planned to do catheterization and VSD closure.
In the physical examination the patient was full alert, no dyspnoe,
no fever, not anemic, no cyanosis, no edema. he had 8.8 kg of body
weight, 83 cm of body height, 13 cm of arm circumference, and 46.5 cm of
head circumference. From the head examination, the patient had normal
hair, no prominent cheekbone. The patient did not have old man face.
From the eye examination, we found that conjunctiva was not anaemic,
isochoric pupils, diameter 3 mm, positive light reflex, no palpebral edema
and conjunctival pale. There was no abnormalities in the ears, nose and
mouth. There was no increase in jugular vein pressure and no lymph node
enlargement in the neck examination. From chest examination, the ribs
were no clearly visible, symmetrically chest movement, there was no
epigastrial and intercostal retraction, The heart rate was 88 beats per
minute, reguler, grade 3 of 6 pansystolic murmur in the 3rd and 4th left
parasternal line. There was thrill. The respiratory rate was 20 breaths per
minute, reguler, and there were no rales and wheezing. There was breath
sound same in all region both left and right lung. From the abdomen
examination, there was no distension, normal bowel sound, no shifting
dulness, tympanic sound. Liver and spleen was not palpable. From the
limb examination, there was normal limit.
The extremities was warm, pulse was 88 beats per minute, same
quality in the four extremities, reguler, but weak. Capillary refill time was
less than 2 seconds, oxygen saturation 94-96% in four extremities, and the
blood pressure was 90/50 mmHg (P50th - P95th : 85-100/ 37-53 mmHg )
Table 1. Laboratory Examination
6/4 Reference
Hb (g/dL) 10.7 12 – 16
Ht (%) 33 36 – 47
Leukocyte (/mm3) 10.570 4000 – 11000
RDW(%) 13.8% 11-15
Eosinophil (%) 10.1 1–3
Basophil (%) 0.4 0–1
Neutrophil (%) 65.5 50 – 70
Lymphocyte (%) 19.2 20 – 40
Monocyte (%) 4.8 2–8
Natrium (mEq/L) 136 135 – 155

Kalium (mEq/L) 4,4 3.6 – 5.5
Chloride (mEq/L) 105 96 – 106
Blood glucose(mg/dL) 82 <200
Ureum (mg/dL) 26 19 – 44
Creatinin 0.44 0.6 – 1.1
SGOT ( U/L) 41 5-34
SGPT ( U/L) 15 0-55
PT
- Patient 12.3
- Control 14.0
INR 0.84
APTT
- Patient 24.7.
- Control 33.7
TT
- Patient 20.4
- Control 19.0
HBsAg Non reaktive

Anti HIV ( 3 methode) Non reaktive
On that day, patient were done chest x-ray. From that examination cardio-
thoracic ratio <50%, no infiltrate in both lungs. Patient was diagnosed with
congenital heart failure ROSS I-II with VSD-DCSA plus mild malnutrition.
Physical examination when receiving this patient (8th April 2018)

General examination
Patient was fully alert, no short of breathness, afebrile. There was no
anemic, no edema, no dyspnoe and no jaundice.
Vital sign:
 Temperature : 36.70C
 Heart beat : 90 beats per minute
 Respiratory rate : 18 breaths per minute
 Blood pressure : 90/50 mmHg
Conclusion : normal vital sign
Nutritional status and anthropometry:
Body weight for age: 8.8 kg (between -3 and -2 SD,WHO 2006 growth
chart), Height for age : 83 cm (between -2 and 0 SD, WHO 2006 growth
chart), weight for Height : 8.8 kg and 83 cm ( between -3 and -2 SD,
WHO 2006 growth chart), Height age : 1 years and 7 months (WHO
2006 growth chart), Ideal body weight : 11.3 kg, Mid upper arm
circumference: 13 cm (between 3th and 15th percentile Frisancho curve)
Head circumference : 47 cm (between -2 and 2 SD WHO Nellhaus curve)
Conclusion: mild malnutrition
Specific examination
- Head :
There was normal hair, and no old man face. Eye : conjunctiva was
not anaemic, isochoric pupils, diameter 3 mm, positive light reflex, no
palpebral edema and subconjunctival bleeding. Ears : no discharge
Nose : no nasal flare, no nasal discharge
Mouth : no cyanosis in the lips and tongue
- Neck : no increased jugular vein pressure, no lymph node enlargement
- Chest : no lag of chest movement. there was no retraction, The heart
rate was 90 beats per minute, reguler, grade 3 of 6 pansystolic
murmur in the 3rd and 4th left parasternal line. There was thrill.
The respiratory rate was 18 breaths per minute, reguler, there was no
rales and no weakness of lung breath sound. There was breath sound
same in all region both left and right lung
- Abdomen examination : no distension, normal bowel sound, no shifting
dulness, tympanic sound. Liver and spleen was not palpable.
- Limb : The extremities was warm, pulse was 90 beats per minute,
same quality in the four extremities, reguler, and strong. Capillary refill
time was less than 2 seconds, oxygen saturation 94-96% in four
extremities, and the blood pressure was 90/50 mmHg.
III. Summary
MZ, a 1 years 8 months old girl, came to pediatric cardiology clinic A
Hospital due to easily tired since 3 months before admission, hardly
achieved weight gain, with history of shortness of breath and recurrent
chronic cough since he was 1.5 months old. From echocardiography when
he was 1.5 months old, he was diagnosed with VSD and routinely
checked-up every month and did echocardiography every 6 months.
Patient advised to undergo VSD closure when he achieved sufficient body
weight.
On the physical examination, he was full alert, no dyspnoe and no
cyanosis condition. he had no nasal flare,no cyanotic in lips and tongue,
no increased jugular vein pressure, chest no retraction, no tachycardia,
no tachypnea. There were no rales, no wheezing. The were thrill and
pansystolic murmur grade 3 of 6 in the 3rd and 4th left parasternal line.
the laboratory examination result was normal limit, chest x-ray result was
normal. the echocardiography confirmed the previous diagnosis of VSD
with DCSA 3-3.2 mm. This patient had been treated with antifailure drug.
IV. Differential Diagnosis

- Congestive heart failure (I50.2) ROS I-II + VSD-DCSA (Q.21.0)
+ Mild malnutrition (E44.1)
V. Working Diagnosis
Congestive heart failure (I50.2) ROS I-II + Ventricle septal defect ,
DCSA + Mlid malnutrition (E44.1)
VI. Problem list

1. Congestive heart failure
 Diagnosis was based on clinical symptom and sign
 Management :
- Treat main problem (ventricular septal defect – doubly commited
subarterial)
- administered diuretic drug and restricted fluid balance
- diet with targeted calori 1130 kcal/kg/day
2. Ventricular septal defect and Doubly commited subarterial
 Diagnosis was established by echocardiographic examination
 Management : transcatheter defect closure with device.
Penutupan septal defect secara transkateter dan dengan
menggunakan device untuk ventricle septal defect
 Education :
- About the disease, treatment, and prognosis and treatment
planning
- About side effects and risks of closure procedure.
3. Mild malnutrition
 Diagnosis was based on clinical sign and anthropometry
 Mild malnutrition in this patient was due to many risk factors such
as, her congenital heart disease, hypoxia, and intake. The
correction of her main disease is the primary management to
improve the nutritional status in addition to adequate nutrition
4. Immunization
There is no absolute contraindication in giving immunization in mild
malnutrition. We should give the immunization in this patient when
he is in the stabil condition.
VII. Management plan

a. Congestive heart failure
Non pharmacologic
- Bed rest
Pharmacologic therapy plan
Anti congestive heart failure
- Furosemide 2 x 10 mg
- Spironolactone 2 x 12.5 mg
b. Ventricular septal defect and Doubly commited subarterial
- VSD closure
c. Pediatric nutritional management
- Nutrition problem : Mild malnutrition
- Calorie requirement : RDA x IBW = 1130 kkal
- Nutritional intake : Oral
- Food type : Regular meal 3 times 750 kkal , snack 2 times, high
calorie milk 3 x 125 cc
d. Evaluation of response and tolerance to intake, monitoring of
weight, fluid balance, and edema
e. Planning of consult
- Consult anesthesiology department
- Consult to Nutrition and metabolic disease division
- Consult to social pediatric
f. Monitoring plan
- Monitoring general appearance and vital sign
- Monitoring signs of heart failure
- Monitoring nutritional intake, fluid intake, fluid balance, and diuresis.
g. Education plan
- Explanation about diasease, therapy,prognosis and side effect of
therapy to parents.
- Explanation to others action plan.
- Explanataion of complication and therapy given.
- Motivised patient to take the therapy.
- Motivised the patient to take care healthy and higienity.
- Motivised the family to give mental and emotional support to the
patient
- Motivised the pastient and parents to get the well nourishment.
h. Monitoring plan
- Monitoring general appearance and vital sign
- Monitoring signs of heart failure
- Monitoring nutritional intake, fluid intake, fluid balance, and
diuresis.
VIII. Follow up
Follow Up Day 1 Follow Up Day 2

(8th April 2018) (9th April 2018)
07.00 07.00
Subjective no dyspnea, no fever, no cough no dyspnea, no fever, no cough
O General Full alert Full alert

appearance
b
Vital sign BP: 90/60 mmHg, HR: 90 bpm, BP: 90/60 mmHg, HR: 88 bpm,
j RR: 18 bpm, temp: 36.70C RR: 18 bpm, temp: 37 0C
SpO2 94-96% SpO2 96-98%
e BW: 8.8 kg BW: 8.8 kg
c Physical Head: no anemic conjunctivae, no icteric sclerae Head: no anemic conjunctivae, no icteric sclerae
examination Neck : no increase JVP Neck : no increase JVP
t Chest : Symmetrical, no lag of movement, no epigastrial Chest : Symmetrical, no lag of movement, no epigastrial
i retractions, look thrill retractions, look thrill
Lung: vesicular sound, no additional sounds in both of Lung: vesicular sound, no additional sounds in both of
v lungs lungs
Heart: pansystolic ejection murmur grade 3/6, ICS Heart: pansystolic ejection murmur grade 3/6, ICS
e
3-4 left parasternal line 3-4 left parasternal line
Abdomen: no distension, normal peristaltics, Abdomen: no distension, normal
no hepatosplenomegaly peristaltics, no hepatosplenomegaly
Extremities: no edema, warm acrals, good perfusion. Extremities: no edema, warm acrals, good perfusion.
Fluid balance Fluid balance: - 10 ml Fluid balance: - 30 ml
/Diuresis Diuresis: 1.1 ml/kg/hour Diuresis: 1.3 ml/kg/hour
Laboratory - -
examination
Assessment 1. Congestive Heart Failure ROS I-II 1. Congestive Heart Failure ROS I-II
2. Ventricle septal defect- DCSA 2. Ventricle septal defect- DCSA
3. Mlid malnutrition 3. Mlid malnutrition
a Pharmacologic -Furosemide 2 x 10 mg, Spironolactone 2 x 12.5 mg -Furosemide 2 x 10 mg, Spironolactone 2 x 12.5 mg
n
Diet 3 times regular meal + 2 times snack + 2 x 100 cc high 3 times regular meal + 2 times snack + 2 x 100 cc high
calorie milk calorie milk
Intervention Planned for catheterization and correction venctricular Planned for catheterization and correction venctricular
septal defect septal defect
Pediatric social : result of denver was according of age
PedQl showed that is often problem to disease and
treatment
07.00 07.00

appearance
b
Vital sign BP: 90/60 mmHg, HR: 92 bpm, BP: 90/60 mmHg, HR: 90 bpm,
j RR: 18 bpm, temp: 36.90C RR: 20 bpm, temp: 37 0C
SpO2 96-98% SpO2 94-96%
e BW: 8.8 kg BW: 8.9 kg
c Physical Head: no anemic conjunctivae, no icteric sclerae Head: anemic conjunctivae, no icteric sclerae
i retractions, look thrill retractions, look thrill
v lungs lungs
Heart: pansystolic ejection murmur grade 3/6 ICS Heart: pansystolic ejection murmur grade 3/6 ICS
e
3-4 left parasternal line 3-4 left parasternal line
Abdomen: no distension, normal peristaltics, Abdomen: no distension, normal
Extremities: no edema, warm acrals, good perfusion Extremities: no edema, warm acrals, good perfusion
Fluid balance Fluid balance: - 20 ml Fluid balance: +15 ml
/Diuresis Diuresis: 1.2 ml/kg/hour Diuresis: 1.1 ml/kg/hour
Laboratory - -
examination
4. Post VSD closure
P Pharmacologic -Furosemide 2 x 10 mg, Spironolactone 2 x 12.5 mg - Furosemide 2 x 10 mg, Spironolactone 2 x 12.5 mg,
l aspilet 1x40 mg
a
n Intervention Planned for catheterization and correction venctricular - Evaluation murmur and dorsalis pedis pulses
septal defect - Evaluation hematoma at puncther catheterization
l Consult to anesthesia - Evaluation echocardiogrphy at 1 and 7day post
closure
- Evaluation echocardiography continous at 1, 3, 6
month
07.00 07.00

appearance
b Vital sign BP: 90/60 mmHg, HR: 92 bpm, BP: 90/60 mmHg, HR: 92 bpm,
j RR: 18 bpm, temp: 36.90C RR: 18 bpm, temp: 36.90C
SpO2 96-98% SpO2 96-98%
e BW: 8.9 kg BW: 8.9 kg
c Physical Head: anemic conjunctivae, no icteric sclerae Head: anemic conjunctivae, no icteric sclerae
retractions, look thrill retractions, look thrill
i
v lungs lungs
Heart: no murmur Heart: no murmur
e Abdomen: no distension, normal peristaltics, Abdomen: no distension, normal
Extremities: no edema, warm acrals, good perfusion Extremities: no edema, warm acrals, good perfusion
Fluid balance Fluid balance: +15 ml Fluid balance: +20 ml
/Diuresis Diuresis: 1.1 ml/kg/hour Diuresis: 1 ml/kg/hour
Laboratory - Hb : 9.9 g/dL -
examination - Ht : 32 %
- Leucosit :9.850
- Trombosit : 311.000 /uL
echocardiography post transchateter VSD closure
: device insitu, small residu VSD (1 mm), no AR,AS ),
dialted LA-LV, good contractility ( EF 71%,FS 39%)
4. Post VSD closure 4. Post VSD closure
P Pharmacologic -Furosemide 2 x 10 mg, Spironolactone 2 x 12.5 mg, -Furosemide 2 x 10 mg, Spironolactone 2 x 12.5 mg,
l aspilet 1x40 mg aspilet 1x40 mg

a
n Intervention -Evaluation murmur and dorsalis pedis pulses -Evaluation murmur and dorsalis pedis pulses
-Evaluation echocardiografi pada 7 hari post penutupan -Evaluation echocardiografi pada 7 hari post penutupan
-Evaluation sign of hemolysis -Evaluation sign of hemolysis
Follow Up Day 7
(14th April 2018)
07.00
Subjective no dyspnea, no fever, no cough
O General appearance Full alert
b
Vital sign BP: 90/50 mmHg, HR: 88 bpm,
j RR: 18 bpm, temp: 36.90C
SpO2 96-98%
e BW: 9 kg
c Physical examination Head: anemic conjunctivae, no icteric sclerae
Neck : no increase JVP
t Chest : Symmetrical, no lag of movement, no epigastrial retractions,
i look thrill
Lung: vesicular sound, no additional sounds in both of lungs
v Heart: no murmur
Abdomen: no distension, normal peristaltics, no
e
hepatosplenomegaly
Extremities: no edema, warm acrals, good perfusion
Fluid balance /Diuresis Fluid balance: +15 ml
Diuresis: 1.5 ml/kg/hour
Laboratory examination -
Assessment 1. Congestive Heart Failure ROS I-II
2. Ventricle septal defect- DCSA
3. Mlid malnutrition
4. Post VSD cosure
P Pharmacologic -Furosemide 2 x 10 mg, Spironolactone 2 x 12.5 mg,
l aspilet 1x40 mg
Diet 3 times regular meal + 2 times snack + 2 x 100 cc high calorie milk
a Intervention -Evaluation murmur and dorsalis pedis pulses
n -Evaluation echocardiografi pada 7 hari post penutupan
- out patient and planning of immunization cath up
IX. Prognosis (Ad vitam, ad functionam, ad sanationam)
- Ad vitam: dubia et bonam
- Ad functionam: dubia et bonam
- Ad sanationam: dubia et bonam
X. Disease Course Timeline
Juni 2016 5th April 2018 6th April 2018 8th April 2018 14th April 2018
Policlinic Observation Observation

Firstly Hospitalizatio
started ended
diagnosed cardiology n
VSD
XI. Case analysis
Physical examination
Anamnesais - Dyspnoe of effort

- Murmur sound, thril Medical Test
 Fatigue - Wasted, underweight 1. -Laboratory : Routine blood,
 History of recurrent breathlessness
 History of recurrent of Cough RFET,LFT,electrolyte
 Feeding difficulty 2. -Imaging :
 Diaphoresis 3. Chest x-ray: normal, CTR<50%
 Poor Weight gain 4. Echocardiography: VSD-DCSA 3-3.2
 Birth of preterm mm
5. Dilated LA-LV,
Diagnosis
 Congestive heart failure ROS I-II
 VSD-DCSA
 Mild malnutrition
Management
Heart Failure ROS I-II Ventricular septal defect - DCSA Mild malnutrition
- Diuretic - VSD closure - Nutrional administration
Observation
- Tolerance and
acceptability
Observation Observation Follow up post VSD closure
- Anthropometry
- -Clinical
- Vital sign -Echocardiography - -Phycal examination
- Fluid balance - -Echocardiografi
- -Pulses arteri dossalis pedis
Prognosis
- Ad vitam : ad bonam
- Ad functionam: ad bonam
- Ad sanationam:dubia ad bonam
(Level of evidence 1)
XII. Discussion
Ventricular septal defect (VSD) is a developmental defect of the
interventricular septum resulting from a deficiency of growth or a failure of
alignment or fusion of component parts of ventricular septum. Isolated
ventricular septal defect occurs in approximately 2-6 of every 1000 live
births and accounts for more than 15-20% of all congenital heart
diseases1.
VSD can be classified according to the location of the defect by
anatomically. VSD classification based on location of defect: VSD
perimembrenous, muscular, doubly committed subarterial also called
oriental type. Based on its physiology VSD can be classified into: small
defects with normal pulmonary vascular resistance; mild defect with
pulmonary vascular resistance varies; large defect with low-mild
pulmonary vascular resistant increases, large VSD with high pulmonary
vascular resistant.2 According to magnitude the size of defect is divided
into a small VSD (<5 mm), moderate (5-10 mm) and large> 10 mm.3
Based on echochardiograpy, patient has been diagnosis of congenital
heart disease type small VSD-DCSA with 3-3.4 mm diameter
VSD is the most common type of major human birth malformation,
affecting approximately 1.5-3.5 per 1,000 live births.4 Most forms of
congenital heart disease, including ventricular septal defect, have
multifactorial origins. An underlying inherited genetic predisposition could
act synergistically with epigenetic factors, direct and indirect environmental
causes cardiac anomalies. Environmental factors such as teratogens,
maternal infections, and untreated maternal metabolic illnesses (eg,
phenylketonuria and pregestational diabetes) have been associated with
ventricular septal defect.5 Behavior factor such as smoking, alcohol
ingestion have been reported to both cause birth defect and be risk for
preterm birth.6 study in china in 2013 reported that prevalence rate ratio of
congenital heart defect was higher in twin, multi-fetal infants, mothers over
30 years of age, mothers with ≥3 parity. The risk for congenital heart
defect among live infants was positively associated with family history of
congenital heart defect. 7 while, study Laa et al in Paris show that preterm
birth is associated with an approximately four-fold higher risk of infant
mortality for newborns with congenital heart disease (CHD). This excess
risk appears to be mostly limited to newborns <35 weeks of gestation and
is disproportionately due to early deaths.8 (Level evidence II). Patient born
was prematurely with 35 weeks' gestation and 2600 gram of body weights
that risk factors cause VSD
The clinical findings of patients with a VSD vary according to the
size of the defect and pulmonary blood flow and pressure.4,9 it is unusual
to find symptoms at birth in infants born with VSD. Instead, the symptoms
typically become manifest between the ages of 4 and 8 weeks,
concomitant with the decrease in pulmonary vascular resistance produced
by remodeling of the pulmonary arterioles. Symptoms, however, will occur
much earlier in infants born prematurely.4 Small VSDs with trivial left-to-
right shunts and normal pulmonary arterial pressure are the most
common. These patients are asymptomatic, normal growth and
development. the cardiac lesion is usually found during routine physical
examination.9 With a small VSD, a grade 2 to 5/6 regurgitant systolic
murmur maximally at the left lower sterna border (LLSB) is characteristic.
A systolic thrill may be present at the LLSB. With large VSDs, delayed
growth and development, repeated pulmonary infections, CHF, and
decreased exercise tolerance are relatively common. With a large defect,
an apical diastolic rumble is audible, which represents a relative stenosis
of the mitral valve due to large pulmonary.8
Patients had benn show no symptoms at birth and early symptoms
appear at 1.5 months such as short of breathness, recurrent cough and
lactation, and weight loss. Physical examination found a systolic murmur.
based on echocardiographic results was small VSD diameter 3-3.2 mm.
according to the parents of the 2.7 cm defect size previously .
Heart failure in children is a clinical syndrome caused by low
cardiac output. In children with congenital heart disease and
cardiomyopathy are the most common causes. Some of the causes of
congenital heart failure in children such as left-to-right shunt, valvular
regurgitation, cardiac valve obstruction, or coronary artery insufficiency
can lead to decreased oxygen to the heart muscle. In infant, typical
presentation is characterized by difficulty in feeding, irritability ,cyanosis,
tachypnea, diaphoresis, and growth failure. Fatigue, shortness of breath,
tachypnea, and exercise intolerance, sweating, irritability, raised JVP,
pulmonary crackles, hepatomegally, repeated chest infections, edema and
failure to thrive in children are the main symptoms for children.11,12
The severity of HF in children must be staged according to the Ross
modified classification
1. Class I Asymptomatic
2. Class II Mild tachypnea or diaphoresis with feeding in infants
Dyspnea on exertion in older children
3. Class III Marked tachypnea or diaphoresis with feedin in infants.
Prolonged feeding times with growth failure Marked dyspnea on
exertion in older children
4. Class IV Symptoms such as tachypnea, retractions, grunting, or
diaphoresis at rest.
` The management of congestive heart failure is to eliminate
underlying disease through surgical and non-surgical correction
intervention, treating causes that aggravate symptoms (infection, anemia,
fever) and treatment of heart failure (HF).13 Drugs often used in the
management of heart failure such as diuretics, beta blockers, angiotensin
converting enzyme inhibitors, inotropes, phosphodiesterase inhibitors, and
vasodilators.10 Diuretics therapy plays a crucial role in the treatment of
pediatric patients with HF. The benefits of diuretic therapy include
reduction of systemic, pulmonary, and venous congestion. Spironolactone
may exert additional beneficial effects by attenuating the development of
aldosterone-induced myocardial fibrosis and catecholamine release.
Potential complications of diuretic therapy include electrolyte abnormalities
(hyponatremia, hypo- or hyperkaliemia, and hypochloremia) and metabolic
alkalosis.11 Patients was diagnosed with heart failure ROS I-II and was
given furosemide and spironolactone therapy to treat heart failure.
If medical treatment fails then DSV closure is necessary at any age.
Infants who respond to medical therapy may be operated by 12-18 months
of age. iIndication of DSV closure is uncontrolled heart failure, growth
disorders, recurrent respiratory tract infections, significant left-to-right
shunting with pulmonary systemic compared to systemic (Qp: Qs) ratio
greater than 2:1.2 patient has heart failure, disorder growth and recurrent
respiratory infections.
Doubly committed subarterial VSD occurs more commonly in
Asians, with prolapse of an aortic cusp a common feature.1 Early
intervention is recommended as for this type of VSD.14 Study in Pakistan
in 2015 showed that patients with small restrictive VSD generally been
considered as do not required surgery to a significant percentage (18.7%)
of these patients developed complications later i.e aortic cusp prolaps,
aortic regurgitation, right ventricular track out flow obstruction and
endocarditic.15 ( level eviden II.)
Transcatheter closure of VSD was first reported by Lock et al in
1987 using a Rashkind umbrella device. The Amplatzer muscular VSD
occluder was approved by the US Food and Drug Administration in
September 2007 and by the Taiwan Department of Health in September
2009.16 Closure of the defect may be surgical intervention or cardiology
intervention by using Amplatzer Muscular Ventricular Septal Defect
(AMVO) or Amplatzer Perimembranous Ventricular Septal Defect
Occluder. Transcatheter closure has the advantages of reduced
psychological impact, minimal invasion,short hospital stay,17 obviating
need for cardiopulmonary bypass, minimizing the other complications
relating to surgery, reduced utilization of intensive care resources, and
faster recovery time to normal activities.18 Echocardiograpy was performed
in second post-operative day, the day before discharge and during the
follow-up. The follow-up protocol includes physical examination,
echocardiography, the following 1 week, 1 and 6 months (transthoracic
echocardiography) and yearly thereafter procedure. Patients are routinely
maintained on aspirin 3–5 mg/kg daily or equivalent antiplatelet therapy for
6 months.19 The position and stability of the device, residual shunt or
valve regurgitation, particularly the aortic valve, were carefully checked
during the examination. Procedure-induced valve complications were
defined as new-onset or aggravation of preexisting valve regurgitation
after the procedure.14 The most common complication was residual shunt,
arrhythmia, bradycardia Valvular defect (tricuspid regurgitation, aortic
regurgitation) embolization.18 The incidence of residual shunt immediately
after VSD closure was 5.8% to 7.3%, but it was found to be gradually
reduced in the follow-up.17 systematic review of 37 publications showed
that transcatheter device closure of VSD is safe and yields good result. 18
( Level Eviden based 2.1 ). Patient had closure of VSD and at follow up
found residual shunt with size 1 mm and given aspilet medication after
done closure of VSD.
On physical and anthropometric examination the patient was
diagnosed with mild malnutrition accompanied by congestive heart failure
ROSS I-II. The nutrition needs of children in heart failure describes the
pathophysiology and metabolic implications of this disease. The
prevalence of wasting in pediatric heart failure has been reported to be as
high as 86%, highlighting the importance of nutrition assessment through
all stages of treatment to provide appropriate intake of energy, protein,
and micronutrients. The etiology of malnutrition in pediatric heart failure is
multifactorial and involves hypermetabolism, decreased intake, increased
nutrient losses, inefficient utilization of nutrients, and malabsorption.
Nutrition support, including enteral nutrition and parenteral nutrition,
should be considered an essential part of routine care.20 Malnutrition is
common in children with CHF. Corrective intervention results in significant
improvement in nutritional status on short-term follow-up.21
If the children age is already outside the immunization schedule and
immunization should be given anytime at any age before the child is
exposed to the disease, because he has very little or no antibodies. 22
Malnutrition will decrease cell function immune systems such as
macrophages and lymphocytes. Cellular immunity decreases and humoral
immunity has a low specificity. Although globulin levels are normal or even
elevated, immunoglobulins that are formed can not bind antigens well
because there is a deficiency of the amino acids needed for synthesis of
antibodies. Complement levels are also reduced and macrophage
mobilization is reduced, consequently the response to vaccines or toxoids
is reduced.23 The patient had not been received basic immunization
completely. Immunization and catch up can be given aftar discharge
hospitalization.
The PCQLI should be useful in clinical screening, surveillance, and
evaluation for clinical management children with congenital or acquired
HD. Evaluation of quality of life is important because it allows for better
communication among patients, parents, and health care providers;
prioritization of problems in part on the basis of patient and/or parent
preferences; monitoring of changes over time or in response to specific
therapies; and screening for other significant medical and psychosocial
problems. 24 (level of evidence II-2). Patient had been done PCQL and the
result showed that patient often any problem with disease and treatment.
indicates a problem in the quality of life associated with heart.
XII. Daftar Pustaka
1. Asma Chaudhry T, Younas M, Baig A. Ventricular Septal defect and

associated complications. J Pak Med Assoc, 2011;6:1001-4
2. Pudjiadi AH, Hegar B, Handryastuti S, Salamia Idris N, Ganda Putra
EP, Devita Harmoniati E. Pedoman pelayanan medis IDAI. Jakarta :
IDAI.2009.h.38-40
3. Soeroso S, Sastrosoebroto H. Penyakit jantung bawaan non-sianotik.
Dalam: Sastroasmoro S, Madiyono B. penyunting. Buku ajar kardiologi
anak. Edisi kesatu. Jakarta: Ikatan Dokter Anak Indonesia. 1994.
h.191- 233
4. Spicer DE, Hsu HH,Co Vu J, Anderson RH, Frickel FJ. Ventricular
septal defect. Orphanet Journal of Rare Diseases.2014;9:144.
5. Penny DJ, Vicky GW III. Ventricular septal defect.
Lancet.2011:377:p1103-12.
6. Swanson, Sinkin. Congenital birh defect. In: Raju TN, Jain L. Editor.
Moderate Preterm, Late Preterm, and Early Term Births: philadelphia.
Elsevier.2013.p639
7. Pei L, Kang Y,Zhao Y, Yan H. Prevalence and risk factors of congenital
heart defects among live births: a population-based cross-sectional
survey in Shaanxi province, Northwestern China. BMC
Pediatrics.2017.17;18:1-8
8. Laas E, Lelong N, Ancel PY, Bonnet D, Houyel L, Magny JF. Impact of
preterm birth on infant mortality for newborns with congenital heart
defects: The EPICARD population-based cohort study.BMC
Pediatrics.2017.17;124:1-8
9. D, Bernstein. Ventricular septal defect. In: Kliegman RM, Stanton BF,
St.Geme III JW, Schor NF, Behrman RE, editors. Nelson textbook of
pediatrics. 20th ed. Philadelphia: Elsevier. 2016: p. 2194-6
10. Park MK. Ventricular Septal Defect. In: Park MK, Salamat M,
Penyunting. Park’s The Pediatric Cardiology Handbook.Edition 5.
Philadelpia: Elsevier. 2016.p.102-8
11. Masarone D, Valente F, Rubino M, Vastarella R, Gravino R,
Alessandra Rea A et al. Pediatric Heart Failure: A Practical Guide to
Diagnosis and Management. J PedNeo. 2017.p.1-10
12. Hussain M, Hussain S, Krishin J, Abbasi S.Presentation of congestive
cardiac failure in children. J Ayub Med Coll Abbottabad.2010;22:135-
138
13. M, M Djer. Gagal jantung anak. Materi program online simposium
IDAI. Jakarta:IDAI. 2013.hal 73
14. Zhang S, Zhu Da, Qi An, Hong Tang, Dajiang Li, Ke Lin. Minimally
invasive perventricular deviceclosure of doubly committed sub-arterial
ventricular septal defects: single center long-term follow-up results.
Journal of Cardiothoracic Surgery.2015;10:1-7
15. Hyder SN, Kazmi U, Kazmi T. Small Ventricular septal defect
considered not requiring surgical closure: The Frequency of
developing Complications in our center.Heart Res Open J.
2016;2:144-9.
16. Ching YF. Transcatheter Device Closure of Muscular Ventricular
Septal Defect. Pediatrics and Neonatology.2011;52:3-4.
17. Liu Jun,Wang Z, Gao L,Lian Tan H, Zheng Q, Zhang ML. A Large
Institutional Study on Outcomes and Complications after
Transcatheter Closure of a Perimembranous-Type Ventricular Septal
Defect in 890 Cases. Acta Cardiol Sin.2013;29:271-76.
18. Yang L, Tai BC, Kin LW, Quek SC. A Systematic Review on the
Efficacy and Safety of Transcatheter Devic. Journal of Interventional
Cardiology.2014;27:260-72.
19. Ching Fu Y, Ling Cao Q, Hijazi ZM. Closure of perimembranous VSD
using the Amplatzer membranous VSD occluder. In Shakeel A
Qureshi, wilson N, Ziyad M Hijazi Horst Sievert: Editor. Percutaneous
Interventions for Congenital heart disease. Informa
healthcare.2007.p361
20. Lewis KD, Conway J, Cunningham C, Bodil M. Larsen K. Optimizing
Nutrition in Pediatric Heart Failure: The Crisis Is Over and Now It’s
Time to Feed. Nutrition in Clinical Practice.2017.p1-6.
21. Vaidyanathan B, Nair SB, Sundaram KR, Suresh GR, Kumar RK.
Malnutrition in Children with Congenital Heart Disease (CHD):
Determinants and Short-term Impact of Corrective Intervention.Indian
Pediatric.2008;45:541-46.
22. Musa DA, Sitaresmi MN. Jadwal imunisasi tidak teratur. Dalam: Ranuh
IGN, Hadinegoro SRS, Kartasasmita CB, Ismoedijanto, Soedjatmiko,
Gunardi H, Hendrarto TW, editors. Pedoman imunisasi di Indonesia.
6th ed. Jakarta: Badan Penerbit IDAI. 2017: p. 65-9.
23. Prendergast AJ. Malnutrition and vaccination in developing
countries.Phil Trans R Soc. 2015; 370:1-8.
24. Marino BS, Tomlinson RS, Wernovsky G, Drotar D, Newburger JW,
Mahony L. Validation of the pediatric cardiac quality of life inventory.
Pediatrics. 2010;126:498-508
Daftar jurnal yang digunakan untuk EBP (4 jurnal):

1. Yang L, Tai BC, Khin LW, Quek SC. A systematic review on the
efficacy and safety of transcatheter device closure of ventricular
septal defects (VSD). J Interv Cardiol, 2014, 27(3):260–272.
1. Best KE, Rankin J. Long-term survival of individuals born with
congenital heart disease: A Systematic Review and Meta-Analysis.
J Am Heart Assoc. 2016;5:1-16
XII. Abbreviation List
DCSA : Doubly committed subarterial

LA : Left atrium
LV : Left ventricle
VSD : Ventricular Septal Defect
CTR : Chest thorax ratio
CHD : Congenital heart disease
LLSB : Left Lower sterna border
JVP Jugular venous pressure
HF : Heart Failure
PCQL : pediatric cardiac quality of life
Hb : Hemoglobin
Ht : Hematokrit
WBC : White Blood Cell
ECG : Elektrocardiography
VSD : Ventricular Septal Defect
RDA : Recommended Dietary Allowance
IBW : Ideal Body Weigh
Kg : kilogram
Cm : centimetre
Inj : Injection
EBP : Evidence Based Practice
WHO : World Health Organization
Appendix
Z Score WHO Curve
Upper Arm Circumference
Nellhaus Head Circumference C
Birth day : 25 January 2016 1 years 8 mont ,
Head circumference : 47 cm
MZ

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Patient Case Report

The condition before observation

Natrium (mEq/L) 136 135 – 155

Blood glucose(mg/dL) 82 <200

HBsAg Non reaktive

Physical examination when receiving this patient (8th April 2018)

IV. Differential Diagnosis

VI. Problem list

VII. Management plan

Follow Up Day 1 Follow Up Day 2

Subjective no dyspnea, no fever, no cough no dyspnea, no fever, no cough

O General Full alert Full alert

a Pharmacologic -Furosemide 2 x 10 mg, Spironolactone 2 x 12.5 mg -Furosemide 2 x 10 mg, Spironolactone 2 x 12.5 mg

Subjective no dyspnea, no fever, no cough no dyspnea, no fever, no cough

O General Full alert Full alert

Subjective no dyspnea, no fever, no cough no dyspnea, no fever, no cough

O General Full alert Full alert

l aspilet 1x40 mg aspilet 1x40 mg

Subjective no dyspnea, no fever, no cough

O General appearance Full alert

Policlinic Observation Observation

Anamnesais - Dyspnoe of effort

- Diuretic - VSD closure - Nutrional administration

1. Asma Chaudhry T, Younas M, Baig A. Ventricular Septal defect and

Daftar jurnal yang digunakan untuk EBP (4 jurnal):

DCSA : Doubly committed subarterial

Z Score WHO Curve

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