PPT LAPORAN KASUS INTERNA VSD LALE SIRIN.pptx

26 Year Old Adult with
Ventricular Septal Defect (VSD)
Lale Sirin Rifdah Salsabila
H1A322107
Supervisor : Dr. dr. Yusra Pintaningrum,
Sp.Jp(K), FIHA, FAPSC,FAsCC,FAPSIC
CASE REPORT

TABLE OF CONTENTS
Introduction
01.
Case Report
03.
02.
Literature Review Discussion
04.
Conclusion
05.

INTRODUCTION
Cardiovascular disease is the leading cause of death worldwide and significantly contributes to
morbidity and increased health costs1. Structural heart disease accounts for a sizeable
proportion of the overall burden of cardiovascular disease, especially in low- and middle-
income countries3.
Ventricular septal defect (VSD) is a structural abnormality of the heart characterized by a
defect in the septum that separates the two chambers of the heart (interventricular septum) 3.
Most of VSD is congenital, in a few case it can be acquired due to trauma, surgery, or
complications of other diseases such as myocardial infarction and infective endocarditis4–6.

Definition
Ventricular Septal Defect (VSD) is a heart structural disorder characterized by a defect
in the septum that separates the two chambers of the heart (interventricular septum).
It consists of the following four components11 :
1. Inlet (atrioventricular canal septum) : This portion extends posteriorly from
the membranous portion to the posterior wall of the heart thereby closing the
gap between the two atrioventricular valves
2. Trabecular : characterized by the presence of trabeculations which are then
divided into three parts ( apical, mid muscular, high muscular)
3. Outlet (infundibular or conal) : Extends anteriorly from the membranous pars
to the superventricular crest.
4. Membranous : is a fibrous. It faces the tricuspid valve and the small portion of
the right atrium on the right and the left ventricular outflow tract.
Figure 1. Schematic of the components of the
interventricular septum 11

Definition
Figure A. A double outlet right ventricle with the aorta
arising exclusively from the right ventricle with a cranial
margin formed by a fibrous continuity between the aortic
and mitral valve outlets. it can never be closed because such
a closure would block the aorta from the left ventricle.
Figure B. The yellow dots on the image indicate the
edges of the defect can be closed thereby placing the
aortic root in continuity with the left ventricular cavity.

Etiopathogenesis
Congenital VSD : developmental abnormalities or impaired formation of the
interventricular septum during cardiac organogenesis. Can occurs alone or coexist
with other congenital heart defects (ex: atrial septal defect (ASD), patent ductus
arteriosus (PDA), right aortic arch, pulmonary stenosis, Tetralogy Of Fallot (ToF) and
Transposition Of The Great Arteries (TGA)) 9
Most VSDs are congenital. Few case can be acquired as : a result of trauma, surgery, or
complications of other diseases such as myocardial infarction and infective
endocarditis4–6.

Etiopathogenesis
Several GENETIC FACTORS that can caused VSD :
- Chromosomal
- single gene, and polygenic inheritance.
- TBX5 mutations in patients with Holt-Oram syndrome
- Maternal infections (rubella, influenza, and febrile illness)
- aternal diabetes mellitus
- Penylketonuria
- Exposure to toxic substances (alcohol, marijuana, cocaine, and certain
drugs such as metronidazole and ibuprofen)

Etiopathogenesis
1 2 3 4 5
VSD on the other hand can also be a sequela of blunt trauma, pathophysiology :
Compression of the heart between the
sternum and vertebrae
Increase in intrathoracic pressure at the
end of diastole or early systole
The ventricles are filled while the valves
are being closed.
Myocardial contusion (most commonly),
coronary artery dissection or adventitial
bleeding occurs.
Necrosis and rupture of
the interventricular
septum
The most common site of injury is the interventricular septum pars muscularis near the apex of the heart. In
addition, significant blunt chest trauma can also reopen closed septal defects in patients with congenital
VSDs.

Epidemiology
1,5 - 3,5 / 1000
Incident of congenital VSD :
of all congenital heart disease in children.
live births
37%
VSD most often affects the membranous part of the interventricular
septum (70%), while the rest are located in the muscularis part (30%).

Classification
- Type 1 : (infundibular, outlet) VSD is located below the semilunar
(aortic and pulmonary) valves in the outlet septum of the right
ventricle above the crista supraventricularis, therefore it is also
sometimes referred to as supracristal.
- Type 2 : (membrane) VSD is by far the most common type,
accounting for 80% of all defects. The defect is located in the
membranous septum inferior to the supraventricular crista and
often involves the muscular septum commonly known as the
perimembrane.
- Type 3 : (atrioventricular canal or inlet) VSD is located just
below the inlet (tricuspid and mitral) valves within the inlet
portion of the right ventricular septum.
- Type 4 : (muscular, trabecular) VSD is located on the muscular
septum, bounded by muscle usually at the apical, central, and
outlet portions of the interventricular septum. Can be multiple
resulting in a "Swiss Cheese" appearance.

Diagnosis Enforcement
Symptom
Patients with large VSDs
develop CHF in early
childhood due to LV fluid
overload and severe PAH.
Symptoms: rapid breathing,
refusal to feed, failure to thrive,
and frequent lower respiratory
tract infections.
VSD patients with
complications of pulmonary
vascular disease and right-to-
left gout symptoms: tightness
and cyanosis. Infective
endocarditis can occur
regardless of the size of the
defect.
Physical
Examination
- VSD murmurs (usually pan-
systolic best heard at the
left lower sternal border)
- Diastolic decrescendo
murmurs and a wide pulse
pressure (detected in cases
of aortic regurgitation).
- Increase LV outflow may
cause a mid-diastolic
rumbling sound at the left
lower sternal border.
- Eisenmenger syndrome:
cyanosis, desaturation,
dyspnea, syncope,
secondary erythrocytosis,
and clubbing
- Systolic thrill

Supporting
Examination
- Chest X-ray
- ECG
- Echocardiography with
Color Doppler
- CTA/MRI
- Cardiac catheterization
Chest X-ray: normal or cardiomegaly,
increased bronchovascular markings, and
atelectasis of the left lower lung lobe.

ECG: completely normal in half of the patients with VSD. Some
case may show left, right pr both ventricular hypertrophy. In
patients with PAH, the ECG may show right bundle branch block,
right axis deviation, and right ventricular (RV) hypertrophy and
dilatation.
Supporting
Examination
- Chest X-ray
- ECG
Color Doppler
- CTA/MRI

Echocardiography with Color Doppler: Echocardiogram shows VSD
A cross-sectional echocardiogram taken in a 4-chamber projection
shows the apical VSD (white arrow) on the left side of Figure A. The
right side shows color Doppler of the restrictive hemodynamic state of
the muscular VSD. Apical 5-space view in image B shows color
Doppler of the apical muscular VSD (white arrow).
Supporting
Examination
- Chest X-ray
- ECG
Color Doppler
- CTA/MRI

Echocardiography with Color Doppler: (a) VSD in mid esophageal RV
inflow-outflow view. (b) VSD Inlet VSD in 4-chamber mid-esophageal
view. (c) Subarterial (supracristal/outlet) VSD on the long axis view of
the LV mid esophageal showing right coronary cusp herniation of the
aortic valve. (d) Muscular VSD in 4-chamber mid-esophageal view.
Supporting
Examination
- Chest X-ray
- ECG
Color Doppler
- CTA/MRI

MRI in a patient with a VSD: MRI in a patient with a massive
membranous VSD has not corrected the widening of the inlet causing
Eisenmenger's syndrome.
Supporting
Examination
- Chest X-ray
- ECG
Color Doppler
- CTA/MRI

CTA in a patient with a VSD: CTA in a massive membranous VSD
patient (long arrow). There is a levo-transposition of the large arteries
and a substantial dilatation and morphology of the left ventricle,
which is the origin of the pulmonary artery. After failed gout revision, a
PTPE graft (short arrow) is inserted laterally from the left atrium.
Supporting
Examination
- Chest X-ray
- ECG
Color Doppler
- CTA/MRI

Cardiac catheterization in a patient with a VSD: Useful in patients
who have high pulmonary pressures in order to measure pulmonary
vascular resistance. This study provides further detail about
concomitant aortic regurgitation, in cases of multiple VSDs, and when
coronary artery disease is suspected.
Supporting
Examination
- Chest X-ray
- ECG
Color Doppler
- CTA/MRI

Differential Diagnosis
As part of acyanotic heart disease, the following is the differential
diagnosis of VSD:
- Atrioventricular septal defect
- Atrial septal defect
- Aortopulmonary window
- Coarctation of the aorta
- Pulmonary stenosis
- Cor triatriatum

Treatment
Medikamentosa
- Diuretic : for VSD patients with gout producing symptoms such as failure to thrive, difficulty
feeding, diaphoresis, or tachypnea. When diuretics are used in high doses, side effects, especially
hypokalemia, need to be considered, and potassium-sparing diuretics are selected.
- Afterload reduction is also required to encourage flow direct systemic action of the left ventricle,
thereby reducing the amount of left-to-right gout through the defect. Afterload reduction is
achieved using angiotensin converting enzyme inhibitors (ACEI).
- Inotropic agents such as digoxin are useful in patients with large gout and left ventricular volume
overload. Inotropy with afterload reduction can also be achieved by administering milrinone
intravenously. However, the provision of such therapy is limited to patients awaiting surgery.

Treatment
Antibiotic prophylaxis
Endocarditis prophylaxis is especially indicated in cyanotic congenital heart disease,
previous episodes of endocarditis, and in patients who have prosthetic heart valves or have
been repaired with prosthetic materials.

Treatment
Surgery
Indication for surgical closure according to ACC/AHA guidelines are summarized as
follows:
- Patients suffering from episodes of endocarditis.
- Ratio of pulmonary blood flow to systemic blood flow (Qp/Qs) ≥2 plus clinical evidence
of fluid overload in the LV.
- In milder gout such as Qp/Qs above 1.5, intervention may be considered if there is
evidence of systolic or diastolic LV dysfunction, or if pulmonary artery pressure and
pulmonary vascular resistance are <2/3 of systemic pressure and vascular resistance
respectively systemic.

Prognosis
● About 85% to 90% of Isolated small VSDs close spontaneously during the first year of life. Patients
with asymptomatic small VSDs in the absence of PAH have an excellent prognosis without any
intervention.
● Unrepaired defects >2 cm in diameter are associated with a mortality rate of 71% or late
cardiovascular complications such as pulmonary arterial hypertension. Conversely, the prognosis
is good in VSD patients who have undergone repair.
● Patients still have a higher risk of arrhythmias, endocarditis, and congestive heart failure in the
long term compared to the general population.
● VSD complicated by Eisenmenger syndrome and pulmonary hypertension has a poor prognosis
and is characterized by activity intolerance, hypoxia, and right ventricular dysfunction.
● Traumatic VSD is often life threatening with a mortality rate of 19%.

Complication
● Eisenmenger's syndrome
● Aortic insufficiency due to prolapse
of the aortic valve leaflet
● Infectious endocarditis
● Embolization
● Supraventricular arrhythmias

Patient’s Identity
Nama : Mr. AAG
Gender : Male
Age : 26 yo
Religion : Islam
Ethnic : Sasak
Last education: High school
Adress : Praya
No. MR : 2268XX
Hospitalized date: July 1st 2023
Examination date: July 4th 2023

Patient’s History
Main complaint : shortness of breath
Current medical history :
The patient came to the emergency room RSUDP NTB on July 1st 2023 with complaints of shortness of
breath since 8 am (8 hours before hospitalized). Shortness of breath was felt elapse and it gets worse
when patient start doing activities, even when he walk a few steps. The patient feels more
comfortable in a supine position with the pillow elevated. The patient also had felt nauseous since
this morning but now has improved. Patients often complain of intermittent chest pain. The patient
also complained about his stomach getting bigger and feeling bloated since 1 month ago.
During the examination on July 4 2023 (4th day of treatment) there were no complaints from the patient.
Other complaints such as fever, headache, convulsions, vomiting, abdominal pain, bluish lips were
denied. Urination within normal limit. The patient has not defecated since entering the hospital.

Patient’s History
Past medical history :
- The patient has a history of VSD since a year ago. It was happen because of his chest got hit by a blunt object.
Hypertension, diabetes, high cholesterol, asthma, stroke, liver disease, kidney disease, lung disease, history of
infection and malignancy is denied.
- History of previous operations denied.
Family medical history :
Hypertension, diabetes, asthma, stroke, liver disease, kidney disease, lung disease, history of infection and malignancy
is denied.
Allergy history :
The patient has a history of allergy to demacolin. The patient has no history of food allergies.
Medical history :
Currently the patient is taking furosemide and ramipril from RSUD Praya
Social history :
The patient is an active smoker. The patient has a history of smoking since high school (1-2 packs/day), and frequently
drinks coffee (2-3 cups/day)

Physical Examination
General
condition
Moderate
Awareness Compos mentis (E4V5M6)
BP 120/80 mmHg
HR 89x/mnt
RR 20x/mnt
SpO2 99% RA
Temp
36,5 C

Examination Results
Head
- Inspection: Normocephali, normal hair distribution, lesions (-)
- Palpation: Mass (-), tenderness (-), cephalhematoma (-)
NORMAL
Eye
- Inspection: Conjunctiva anemic (-/-), icteric sclera (-/-), exopthalmus (-/-), eyelid edema (-/-), direct pupillary reflex
(+/+), indirect pupillary reflex (+/ +), isochor, photophobia (-/-)
- Palpation: Tenderness (-/-), palpebral edema (-/-)
NORMAL
Ears
- Inspection: normal shape, symmetrical, normal mucosa, hyperemia (-)
- Palpation: Tenderness (-/-)
NORMAL
Nose
- Inspection: normal shape, symmetrical, septal deviation (-), rhinorrhea (-), bleeding (-), normal mucosa, hyperemia
(-), nostril breathing (-)
- Palpation: Tenderness (-)
NORMAL
Mouth
Inspection: Symmetrical, central cyanosis (-), moist lip mucosa, corner lip lesion (-), stomatitis (-)
NORMAL
Neck
- Inspection: Tracheal deviation (-), mass (-), distended, jugular vein dilatation (-), use of accessory muscles of SCM
breathing (-), hypertrophy of SCM muscles (-)
- Palpation: Trachea is in the middle, lymph node enlargement (-), thyroid enlargement (-), neck stiffness (-)
NORMAL

Percussion:
- Heart boundary: Right border: right parasternal
ICS IV. Left border: ICS V midclavicular left
Auscultation :
- Cor : single regular S1S2, pansystolic murmur on
ICS 3-4 (+), gallop (-)
- Pulmo : Breath sounds (front and back) →
vesicular. Rhonki (-), wheezing (-)
Thorax
Inspection :
- Shape and size of the chest: symmetrical when static, pectus excavatum (-)
- Movement of the chest wall: Symmetrical
- Surface of the chest wall: scar (-), lesion (-), mass (-), spider nevi (-),
gynecomastia (-)
- Use of accessory respiratory muscles: intercostal muscles (-), intercostal
hypertrophy (-), active abdominal accessory muscles (-)
- Ribs and intercostal space: symmetrical, widening between the ribs (-)
- Supraclavicular and infraclavicular fossa: concave, symmetrical
- Jugular fossa: trachea in the middle (+)
- Type of breathing: Thoracoabdominal
Palpation :
- Anterior surface of the chest wall: tenderness (-), mass (-), deformity (-),
crepitus (-) vibration (-), thrill (-)
- Mediastinal position: tracheal deviation (-), ictus cordis palpable at ICS V
MCLS
- Front and back focal fremitus: normally symmetrical
Sonor Sonor
Sonor Sonor
Sonor Sonor

Extremity
- Upper: warm acral (+/+), edema (-/-), deformity (-
/-), cyanosis (-/-), CRT < 2 seconds, clubbing finger
(-/-), koilonychia (-/-)
- Bottom: warm acral (+/+), edema (-/-), deformity
(-/-), cyanosis (-/-), CRT < 2 seconds, clubbing
finger (-/-), koilonychia (-/- )
Abdomen
Inspection :
Distention (+), undulation (+), mass (-), injury (-), dilation of veins (-), blood contour
(-), striae (-)
Auscultation:
Bowel sounds (+) 8x/minute, metallic sound (-)
Percussion:
Tympani entire abdominal field
Palpation:
mass (-), tenderness (-), hepatosplenomegaly (-), CVA tapping pain (-)

Laboratory Examination (1/7/23)
Hemoglobin 11.7 g/dL 12,0-16,0
Leukosit 7.190 /uL 4.000-10.000
Eritrosit 3.88 juta/uL 3,50-5,00
Trombosit 375000 /uL 150.000-400.000
Hematokrit 34 % 25-42
MCV 86,9 fL 80-100
MCH 30,2 pg 26-34
MCHC 34,8 g/dL 32-36
RDW-SD 50,3 fL 35-47
PDW 15,9 fL 9-13
MPV 8.4 fL 7.2-11.1
PCT 0,32 % 0.15-0.40

Basofil 0.09 103/uL 0.00-0.10
Eosinofil 0.46 103/uL 0.00-0.40
Neutrofil 4,83 103/uL 1.50-7.00
Limfosit 1.15 103/uL 1.00-3.70
Monosit 0.66 103/uL 0.00-0.70
Kidney Function
Ureum 40 mg/dL 10-50
BUN 18,69 mg/dL 8,90-20,60
Kreatinin 0,6 mg/dL 0,6-1,3
eGFR 162 ml/mnt/1,73m2 >90

Liver Function
SGOT 51 U/l 0-40
SGPT 75 U/l 0-41
Albumin 2.8 mg/dL 3,5-5,2
Bilirubin Total 0.8 mg/dL <1,00
Bilirubin Direk 0.34 mg/dL <0.20
Elektrolite
Natrium 132 mmol/L 135-146
Kalium 4.2 mmol/L 3.4-5.4
Klorida 100 mmol/L 95-108

Serology
HIV Rapid Non reaktif - Non reaktif

Thorax USG (3/7/23)
Interpretation ::
Efusi pleura bilateral
- Right: volume ± 810 cc, marked on
the midscapular line with a
minimum punctum of ± 2 cm,
punctum optinum of ± 2.4 cm.
- Left: volume ± 845 cc, marked on
the linea midscapula with a
minimum punctum of ± 1.3 cm,
punctum optinum of ± 2.8 cm

Echocardiography (from RSUD Praya)
Echocardiography result :
- VSD subarterial doubly comitted (SADC) diameter 1.5-1.7 cm
- RA-RV dilatasi
- TR minimal, TVs 35-40

ECG (1/7/23)
Interpretation:
- Rhythm : Sinus rhythm
- Pulse Frequency : 102 x/minute
- Axis: Deviation of the axis to the right
- P wave: >120 msec
- QRS complex : Narrow, S/R at V5 = 1.55, SV6 = 8 mm
- ST segment : isoelectric
- T wave : T inversion at AVR, V1, V2
- QT interval : Normal
Impression: Right axis deviation, Left Atrial Enlargement,
Biventricular Hypertrophy

ASSESSMENT
- SADC ventricular
septal defect (VSD).
- Bilateral pleural
effusion

PLANNING
Diagnostic
Echocardiography
Medicamentosa
Inj. Ceftriaxone 1 gr/12 jam IV
Inj. Furosemide 20 mg/8 jam IV
Inj. Lansoprazole 1 x 30 mg IV
Spironolacton pO 1 x 25 mg
Ramipril pO 1 x 2,5 mg
Bisoprolol pO 1,25 mg-0-0
Revatio (Sildenafil) pO 3 x 20 mg
Vipalbumin pO 3 x 1
Non Medicamentosa
O2 nasal cannula 2 lpm
IVFD NaCl 0.9% 500 cc/24 hours
(7 tpm)
Monitor urine output/24 hours
Drink a maximum of 1000 cc /
day

PLANNING
Monitoring
- Monitoring complaints
and vital signs
- Radiology: AP/lateral
chest X-ray
Education
- Explain to patients and families
regarding the disease they are
experiencing
- Explain the risk factors for the
patient's disease
- Explain the diagnostic
approach, management and
complications of the patient's
disease
- Explain the prognosis of the
disease in patients and families
Monitoring
and vital signs
chest X-ray
Monitoring
and vital signs
chest X-ray
Prognosis
Ad Vitam : dubia ad malam
Ad Functionam : dubia ad malam
Ad Sanationam : dubia ad malam

Discussion
This case report describes a 26-year-old man who was diagnosed with a ventricular septal
defect with suspected ADC and bilateral pleural effusion. In Indonesia, it is estimated that of the total
cases of congenital heart disease, 23% of adult cases are VSD. Thus, VSD is the second most common
congenital cardiac anomaly in adults. VSD does not have a sex predilection.
In this case there are two possible causes of VSD. First, congenital VSD that was newly
diagnosed in adulthood, and secondly, VSD was acquired through a blunt trauma mechanism. The
possibility of both tendencies is quite small because traumatic VSD often has a poor prognosis which
causes immediate death. In addition, traumatic VSD often involves the muscularis septum near the apex,
whereas in patients, the location of the VSD is in the infundibular pars.

Discussion
Previous echocardiographic findings suggest the presence of a doubly comitted subarterial
VSD (SADC). SADC VSD is also known as VSD type 1 (infundibular/outlet) which is characterized by a
defect just below the valves of the two great arteries above the supraventricular crest (aortic artery and
pulmonary artery). This type is an unusual type which only represents 6% of all VSDs. However, in Asians
the proportion can reach 30%. This defect does not close spontaneously.
Based on the size comparison with the aortic annulus, VSD can also be divided into small, medium,
and large:
- Small : ≤25%
- Moderate : 25% - 75%
- Large : >75% of the diameter of the aortic annulus.
In this case, the diameter of the VSD is 1.5-1.7 cm. This size then needs to be compared with the normal
value of the aortic annulus in adult males ( 22.3 ± 3.4 mm). Using this reference, it is estimated that the size
of the VSD in patients is in the moderate to severe range.

Discussion
In this case, the patient has come with symptoms of shortness of breath and activity intolerance.
This corresponds to the size of the septal defect in moderate to severe patients. Moderate VSDs result in
moderate LV volume overload and mild PAHs or none at all. As is the case, patients with these defects may
seek treatment at an older age with clinical mild congestive heart failure (CHF).
Smoking is a risk factor for major cardiovascular disease. Congenital heart disease (CHD) patients who
smoke even have an increased risk of dangerous consequences such as coronary heart disease,
hospitalization, and premature mortality. In this case, the patient was known to be an active smoker,
and therefore, adverse side effects may have been influenced by this factor.
Abdominal distention susp. as ascites → Ascites is an abnormal accumulation of fluid in the peritoneal
space. One of the causes is CHF.

Discussion
Hypoalbuminemia in patients with heart failure occurs primarily as a result of decreased albumin
synthesis and protein loss due to hemodilution, chronic inflammatory conditions, hepatic congestion,
malnutrition, cachexia due to fluid overload and proteinuria, or intestinal disease.
Hypoalbuminemia → causing susceptible to infection
The patient's ECG → revealed right axis deviation, left atrial enlargement, and biventricular
hypertrophy.
In patients with PAH, the ECG may show right bundle branch block, right axis deviation, and right
ventricular (RV) hypertrophy and dilatation.

Discussion
Pharmacological treatment : antibiotics, loop diuretics (furosemide), lansoprazole, potassium-sparing
diuretics (spironolactone), ACEI (ramipril), bisoprolol, sildenafil and vipalbumin.
Diuretics → first line of medical palliative treatment in VSD with symptoms.
In addition, afterload reduction is also required to promote direct systemic flow from the left ventricle,
thereby reducing the amount of left-to-right gout through the defect. Afterload reduction is achieved
using angiotensin converting enzyme inhibitors (ACEI).
furosemide → to treat conditions with volume overload and edema secondary to exacerbations of
congestive heart failure.

Discussion
The age-related hazard ratio for mortality in patients with uncorrected VSD was 2.7 (95% CI: 2.4–3.0).
⅓ of these causes of death originate from the heart in patients with uncorrected defects.
Although one-third of these causes are from ischemic conditions, heart failure is the most common non-
ischemic cause.

Conclusion
Ventricular septal defect (VSD) is a disorder in the form of a defect in the
interventricular septum. VSDs are partially congenital, but can also be acquired
from conditions such as myocardial infarction, trauma, or infectious endocarditis.
VSDs are divided into 4 types based on the location of the defect (infundibular,
muscular, membranous, and inlet) and divided into 3 based on the size of the
defect (small, moderate, severe).
Smaller VSDs are sometimes diagnosed in adulthood due to symptoms of
congestive heart failure. Echocardiographic examination is used as the main basis
for the diagnosis of VSD. Correction of VSD either surgically or percutaneously is the
mainstay of treatment. VSD conditions that have been accompanied by pulmonary
vascular disease or Eisenmenger syndrome have a poor prognosis.

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