acyanotic heart disease , ventricular septal defect VSD

1. Case presentation
Dr Aftab Ali
P.G
Baqai medical university

2. Bio data
Name: Khaliq Daad
Age: 1 year
Sex: male
Address: Sohrab Goth Karachi
Date of admission: 18th April 2019
Mode of admission: OPD

3. Presenting complaints
Shortness of breath 4 days
Fever 4 days
Loose motion 3 days

4. H.O.P.I
According to the mother young child has never been in the
state of good health since the age of 4 months every month
she has to visit the doctor for his chest infection now she has
visited our OPD with his short of breath, fever, loose watery
motion. Short of breath associated with mild intercostal
recessions, feeding difficulty and cough without any cyanosis
but fever which is initially low grade then later on high
grade documented 102-103F, intermittent in nature. Not
associated with chills and It is relieved by taking anti-
pyretics.
Mother also complaint of loose motion of grade III for last 3
days not containing blood or mucus and it was associated
with marked irritability, sunken eyes and decrease urine
output for which he has taken treatment from local GP and
found no fruitful with the treatment then she has to come to
Fatima hospital.

5. There is no H/O fits, recurrent vomiting, repeated diarrhea,
repeated ear discharge, recurrent skin infections, he passed
first stool within 24 hours of life. No H/O contact with TB

6. Past History
In past the young child has history of 2 admission 1 in the
private hospital near Sohrab goth and 1 in the govt hospital
for fever and cough, in 1st admission no diagnosis was made
only symptomatic treatment was given, in 2nd admission he
was admitted for 3 days but due to family issue he got
LAMA. Several visit to local doctor for repeated chest
infections.
There is no H/O blood transfusion.

7. Drugs
Syp calpol ¾ Tsf tds
Syp augmentin 156.6mg ½ TSF TDS
Syp Acefyl respiratory ½ TSF TDS
Syp Ceclor 125mg ¾ TSF TDS

8. Birth History
Pre-natal: booked case, antenatal visit done, ultrasound was done,
multivitamins was taken. There is no H/O diabetes mellitus,
Hypertension, swelling of feet, fits during pregnancy. no other drugs
taken, no X-ray done.
Natal: term pregnancy, svd at home by dai.
Post-natal: cried immediately after birth.
no cyanosis, jaundice or fits. Normal birth weight according to
mother.

9. Feeding History
Breast feeding started after 3 hours of birth and exclusive breast feed
for 6 months, weaning started at 6 month with potatoes , khichri.
Required calorie 1000kCal
Before illness calorie taking: 750kcal
During illness taking : 700kcal

10. Immunization
Vaccinated up to age
Last measles's vaccine was given at the age of 9 month
BCG’s scar present.
Vaccination card was at home.

11. Milestones
Gross Motor: can walk holding on to furniture (11 months)
Fine motors: pencil gasp
Hearing and Speech: can say Ba-Ba, Da-Da (9 month) localize near
sound
Social behavior: Drink from cup with assistance

12. Family History
He is product of consangious marriage. Parents are alive and healthy.
Mother’s age is 24 years and Father’s age is 29 years. 1 sister 4 years
old ,healthy.
There is no history of chronic disease like diabetes, asthma, hepatitis
b & c, tuberculosis.
No H/O abortion, neonatal deaths.
No H/O congenital diseases.

13. Social History
Low socioeconomics , father is factory worker.
Own cemented house of 2 rooms , 10 peoples are living. Tap water for
drinking (not boil)

14. General examination
General Impression
An ill looking, irritable male child with no dysmorphic
features of normal build and height lying on bed
uncomfortably with mild intercostal recessions, and having
IV cannula on his left hand.

15. VITALS
R/R: 55 br/mint
Heart rate: 130 beats/mint
Temp.: 102F
B.P: 95/60 mmHg at 50th centile

16. ANTHROPOMETRIC
MEASUREMENT
WEIGHT: 7.8kg below 5th centile
HEIGHT: 73cm above 10th centile
FOC: 41cm below 5th centile
MAC: 13cm

17. Sub-Vitals
anemia: Dehydration: present
cyanosis:
jaundice: Sunken Eyes
clubbing: Dry mucus membrane
koilonychia: Skin pinch goes back
slowly
edema: not present
J.V.P: not raised
Capillary Refill: normal

18. Cardiovascular System
Pulse: 130 b/mint regular rhythm normal volume and normal
character, no radio-femoral delay.
B.P: 95/60 mmHg
Inspection: normal shape, no bulging, no scar, no visible pulsation
Palpation: apex beat was present in 4th ICS medial to midclavicular
line, There were no left parasternal heave, no thrill
Auscultation: S1 and S2 audible at all 4 areas of heart with pancystolic
murmur at left sternal border of grade III, No Radiation, having
blowing character & high pitch.

19. Respiratory System
R/R: 55br/mint
Inspection: normal shape chest, no bulging, no deformity, no visible
vein, no pulsation, no scar mark
Palpation: trachea centrally placed, no tenderness
Percussion: not done
Auscultation: Harsh vesicular breathing with crepts audible on right
side of chest anteriorly.

20. Abdominal Examination
Inspection: abdomen distended, umbilicus centrally placed
inverted, there is no visible vein, pulsation or scar mark.
Palpation: soft, no tenderness, no mass, no visceromegaly
Percussion: no fluid thrill, no shifting dullness
Auscultation: gut sound audible, no bruit

21. CNS examination
State of consciousness: normal
GCS: 15/15
Speech: intact
Cranial nerve: intact
Motor system: Bulk , power, tone and reflexes are
normal .

22. Differential Diagnosis
1. Acyanotic heart disease most likely V.S.D with AGE
with some dehydration
2. Pneumonia
3. Immunodeficiency

23. CBC
TLC: 18.8
N: 80
L: 40
RBC: 4.1
HB: 10.5
HCT: 30
MCV: 72
MCH: 25
MCHC: 34
Platelets: 279

24. RBS
U.C.E
RBS 62
urea 26
creatinine 0.5
sodium 147
potassium 3.5
bicarbonate 26
Chloride 99

25. Urine D/R
Color: Yellow
Specific gravity : 1.015
Albumin: Nil
Sugar: Nil
Red Cells : Nil
Pus cell: 1-2

26. Stool D/R
Pus cells 7-8 cells, watery consistency and no mucus no
blood.

27. X-RAY chest

29. Treatment
Admitted in P.ICU ,
Kept NPO
Input out and TPR charting
O2 given @ 3L/mint
Pulse oximetry and monitor attached and check for oxygen saturation
which was on 94% on 3L
Inj: Ringer lactate 400ml over 4 hours @ 75ml/kg/hour
Inj: 1/5th D/S 500ml over 24hour @ 64ml/kg/hour
Inj: Ceftrixone 100mg/kg in 2 divided doses IV
Inf: paracetamol 10mg/kg/dose 8Hourly
Syp: zinc 1TSF OD
Low osmolar ORS ½ to 1 cup after each loose stool
Probiotics sachet 1 sachet OD P/O given

30. Ventricular Septal Defect

31. Definition
VSD is a developmental defect in the interventricular septum allowing
shunt between the left & right ventricles.

32. Development
➔ At 4-8 weeks of gestation, the single ventricular
chamber is effectively divided into two chambers.
➔ This division is accomplished with the fusion of the
membranous portion of the interventricular septum,
the
endocardial cushions, and the bulbous cordis.
➔ Failure of development or fusion of one of the
above
components during morphogenesis of the
embryonic heart results in a VSD in the
corresponding component.

33. Epidemiology
➔ Most common cardiac
malformation.
➔ It accounts for 25% of all congenital heart disease.
➔ VSDs are the most common lesion in many
chromosomal syndromes, including trisomy 13 (Patau
syndrome), trisomy 18 (Edwards syndrome), trisomy
21 (Down syndrome).

34. Types
According to location of the
defect:
1. Perimembranous (most common)
2. Muscular or Trabecular
3. Outlet VSD (Supracristal/
Infundibular)
4. Inlet VSD (AV canal type)

35. According to size of the defect:
1. Small (<5 mm)
2. Moderate (5-10
mm)
3. Large (>10 mm)
According to haemodynamic
status:
1. Restrictive: Small defect, shunt is limited.
2. Non-restrictive: Large defect, shunt is not
limited.

36. Pathophysiolog
y➔ The pathophysiologic effects of a VSD derive from
the
effects of the left-to-right shunt.
➔ A left-to-right shunt at the ventricular level has
followingHemodynamic
consequences:
◆ Increased LA & LV volume load > LA & LV
hypertrophy
◆ Excessive pulmonary blood flow > Pulmonary HTN
◆ Reduced systemic cardiac output

37. Left to Right shunt
Increased pulmonary blood flow
Endothelial dysfunction & pulmonary vascular remodeling
Increased pulmonary vascular resistance
Inversion of shunt: Right to Left
Eisenmenger’s syndrome
Pathophysiolog
y

38. Natural History
➔ Spontaneous closure occurs in about 50% of cases
by 1
year.
➔ Congestive Cardiac Failure (CCF) develops in
large VSD
after 8 weeks of
age.
➔ In a large VSD, the shunt may reverse as early as
6-12
months of age, but Eisenmenger’s syndrome does
not get established till the teenage years.
➔ Rarely, Infective endocarditis develop in VSD patients.

39. Clinical
Features:
➔ In small defect:
◆ Usually asymptomatic
◆ Normal growth and development.
◆ Incidental detection of a pansystolic murmur at
left 3rd and 4th intercostal spaces.

40. Clinical
Features:➔ Symptoms appear in large defect:
◆ Dyspnoea
◆ Feeding difficulties
◆ Poor weight gain
◆ Easy fatigability
◆ Profuse perspiration
◆ Recurrent respiratory tract infections
◆ Cyanosis is usually absent in early stage

41. Clinical
Features:
➔ General examination:
◆ Appearance: Sick looking, often
malnourished.
◆ Tachypnoea
◆ Tachycardia
◆ Blood pressure: Normal
◆ JVP: May be raised in CCF◆ Pedal oedema: May be present in Heart Failure

42. Clinical
Features:➔ Precordium
examination:
◆ Inspection:
● Hyperdynamic
● May be bulged
◆ Palpation:● Apex beat is thrusting, shifted to the
left.● Left parasternal heave may be
present.
● Thrill may be present in tricuspid
area.
● Palpable P2 may be present.

43. Clinical
Features:➔ Precordium examination:
◆ Auscultation:
● 1st & 2nd heart sounds are audible in all 4
areas
● A harsh, pansystolic murmur (Grade 4/6) best
heard at lower left sternal border at the 3rd, 4th
& 5thintercostal spaces.
● The murmur may radiate to the right lower
sternal
border. Intensity varies based on the size of
the
VSD and pulmonary vascular resistance.

44. Investigations
:➔ Chest X-ray:
◆ In small defects: May be normal.
◆ In large defects:
● Cardiomegaly.
● Increased pulmonary vascular
markings.

45. Investigations
:➔ ECG:
◆ Normal in small defect.
◆ Left ventricular hypertrophy in large VSD
◆ Biventricular hypertrophy when associated
with
pulmonary hypertension.
◆ P wave may be notched when there is left
atrial
enlargement.

46. Investigations
:➔ Echocardiogram:
◆ Shows location & size of the defect.
◆ Shows direction of blood flow.
➔ Cardiac catheterization:
◆ Measurement of intracardiac & intravascular
oxygencontent defines the magnitude & direction of shunting.

47. Treatment:
➔ Counselling:
◆ For small defects:
● Reassurance of parents
● Encouraged to live a normal life
● No restrictions on physical activity
◆ For large defects:
● Parents should be counselled about
itscomplications & prognosis.

48. Treatment:
➔ Medical Management:
◆ Adequate nutrition
◆ Maintenance of good dental hygiene
◆ Antibiotic prophylaxis against Infective
Endocarditis
◆ Treatment of CCF:
● Loop diuretics: Frusemide
● ACE inhibitors: Enalapril, Captopril● Inotropic agents: Digoxin

49. Treatment:
➔ Surgical
Management:◆ As 50% of VSD close spontaneously by 1st year,
patients with small & moderate defects should be
kept
in regular follow-up to observe spontaneous
closure.
◆ In patients with large defects, surgical repair has to
be
done before irreversible damage to the pulmonary
vasculature occurs.

50. Treatment:
➔ Indication of
surgery:
◆ At any age: Patients with large defect in whom
clinical
symptoms & failure to thrive can not be controlled
medically.
◆ <6 months: If patient develops CCF which does
not
respond to decongestive therapy.
◆ After 6 months: Large defects with pulmonary
hypertension, even if the symptoms are controlled
by
medication.

51. ➔ Indication of surgery:
◆ Significant L-R shunt
◆ Patients with a Supracristal VSD of any size should be
operated because of high risk for aortic valve
regurgitation.
➔ Contraindication of surgery:
◆ Large VSD with predominant Right to Left shunt
◆ Small VSD with no CCF
➔ Risk of surgery: The rate of surgical mortality is < 2%

52. Prognosis:
➔ The results of primary surgical repair are
excellent and complications leading to long
term problems are rare.
➔ After surgical obliteration of left to right
shunt:
◆ The hyperdynamic heart becomes quiet
◆ Cardiac size decreases toward normal
◆ Thrills & murmurs are abolished
◆ Pulmonary arterial hypertension
regresses
➔ The long term prognosis after surgery is

53. Complication
sComplications of
VSD:
Complications of
surgery:
➔ Congestive
cardiac
failure
➔ Infection
➔ Post operative
➔
Eisenmenger’s
hemorrhage
syndrome
➔ Aortic
regurgitation
➔ Pulmonary
hypertension
➔ Valve injury
➔ AV block➔ Residual VSD

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