2009-2010

Department of Pediatrics
Prof. Mona El-Samahy unit

Under supervision of:

Prof. Mahmoud Tarek
Dr. Ahmed Samir

Prepared by the fifth year

medical students:
Karim Mohammed
Karim Nagy
Karim Yousry
Kawthar Sayed
Kyrillos Girgis
Kyrillos Raafat
Kyrillos Samir
Lara Ashraf
Lobna Abd El-Fatah
Lobna Ez El-Din

TETRALOGY OF FALLOT
 In The name of The Holy GOD

Presentation

After we finished we realized how great we enrich

our experience!!! .The experience of achieving an
interesting research in a well managed cooperative
teamwork. We tried as much as we can to put this
research in semi-arranged notes. We know! …….this
research isn’t perfect, but it is our first little step
in a very long way….and what we are proud of is
that we have done our best and we were
interested……
Now..!! It’s time for the show…So let’s go…Thanks...!!!

The teamwork,

Cairo, Dec, 2009

 December 6, 2009 [TETRALOGY OF FALLOT]

Index
Introduction ………………………………………………………………………….... 2

Historical origin& Definition ………………………………………..................................... 3

Epidemiology& Etiology& Embryological background…………………………..…..4

Pathophysiology ……………………………………………………………………... 5-6

Clinical picture ………………………………………………………………………... 7-9

Investigations ………………………………………………………………………... 9-11

Complications ………………………………………………………….……………. 11-12

Medical treatment of fallot tetralogy ………………………………...…………. 12

Surgical treatment of TOF ………………………………………………………….. 13-16

References …………………………………………………………………………….. 17

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 December 6, 2009 [TETRALOGY OF FALLOT]

Fallot Tetralogy
Introduction :
*Congenital cardiac defects can be divided into two major groups based on the
presence or absence of cyanosis into:

Congenital acyanotic heart disease

Normal Pulmonary BF(no shunt) Pulmonary Plethora (Lt Rt shunt)
Rt ventricular enlargement Rt ventricular enlargement
 PS  ASD
 MS  PAPVR
Lt ventricular enlargement Lt ventricular enlargement
 AS  PDA
 Coarcotation of Aorta  A-P window
--------------- Biventricular enlargement
 VSD

Congenital cyanotic heart disease

Pulmonary oligaemia Pulmonary plethora
Rt ventricular enlargement Rt ventricular enlargement
 Fallot tetralogy  Hypoplastic left heart syndrome
 VSD + PS  TGA
 VSD + P.atresia (extreme F4)  TAPVR
 DORV + PS
 TGA + PS
Lt ventricular enlargement Rt/Lt ventricular enlargement or both
 Pulmonary atresia  Truncus arteriosus
 Tricuspid atresia  Single ventricle
Huge Rt arium ---------------
 Ebstein anomaly

Classification:
**the fallot tetralogy is one of cyanotic congenital heart lesions with decreased
pulmonary blood flow.

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Historical origin: (6)

Tetralogy of Fallot (TOF) is a congenital heart defect which is classically
understood to involve four anatomical abnormalities (although only three of
them are always present). It is the most common cyanotic heart defect,
representing 55-70%, and the most common cause of blue baby syndrome. It
was described in 1672 by Niels Stensen, in 1773 by Edward Sandifort, and in
1888 by the French physician Etienne-Louis Arthur Fallot, for whom it is
named.
Dr. Fallot
Definition:(6)

Tetralogy of Fallot (TOF) is a congenital cyanotic heart disease, which

is classically understood to involve four anatomical abnormalities
Its four signs are :

1) Ventricular septal defect (figure 1)

2) Pulmonary stenosis , Sometimes the pulmonary valve isn’t just

narrowed but is completely obstructed (pulmonary atresia).

3) Overriding aorta , the aorta lies directly over the ventricular septal
defect .
Figure 1 : ventricular septal defect
4) Right ventricle develops hypertrophy .

*In addition, tetralogy of Fallot may present with other anatomical anomalies, including:
- stenosis of the left pulmonary artery, in 40% of patients
- a bicuspid pulmonary valve, in 40% of patients
- right-sided aortic arch, in 25% of patients
- coronary artery anomalies, in 10% of patients
- a foramen ovale or atrial septal defect, in which case the syndrome is sometimes called
a pentalogy of Fallot,
- an atrioventricular septal defect
partially or totally anomalous pulmonary venous return
forked ribs and scoliosis
- triology of fallot

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 December 6, 2009 [TETRALOGY OF FALLOT]

Epidemiology:(6)

Tetralogy of Fallot occurs in approximately 400 per million live births

Tetralogy of Fallot accounts for 10-15% of all congenital (newborn) heart defects
It is the most common cyanotic heart defect, representing 55-70%,
It occurs slightly more often in males than in females.

Etiology:(6)(7)
*Its cause is thought to be due to environmental as carbon monoxide or genetic factors
or a combination.
*It is associated with chromosome 22 deletions.
*mothers who experience rubella or other viral illnesses during pregnancy have a higher
risk of having a baby with tetralogy of fallot, in addition maternal alcoholism
and diabetes.
*There is higher risk for tetralogy of fallot among white babies than babies of other races
*it may be seen more commonly in patients with Down syndrome (in association with AV
canal defects) , DiGeorge syndrome , Alagille syndrome , charge syndrome ,vacteral
syndrome , fetal alcohol syndrome .

Embryological background :(1)(figue 2)

Tetralogy of Fallot, the most frequently occurring abnormality of the
conotruncal region (Figure. 3), is due to an unequal division of the conus resulting from
anterior displacement of the conotruncal septum.
Displacement of the septum produces the four cardiovascular abnormalities mentioned
before .

Figure 2 :Embryology of TOF Figure 3 : unequal division of the conus

[Department of pediatrics] | Prof. Mona El-Samahy unit 4

 December 6, 2009 [TETRALOGY OF FALLOT]

Trilogy of Fallot: (6)

presented by:
Pulmonary valve stenosis
Right ventricular hypertrophy
Atrial septal defect

Pentalogy of fallot: (8)

Presented by:
The four characteristics of Fallot's tetralogy syndrome, plus a patent foramen

Pathophysiology:
The combination of congenital defects in TOF results
in right to left shunt across the large VSD from the
hypertrophied right ventricle to the overriding aorta
due to obstructed right ventricle outflow tract mixing
of oxygenated and deoxygenated blood in left
ventricle causing persistent arterial desaturation and
cyanosis(5)(figure 4) . The degree of right ventricular
outflow obstruction determines the timing of the
onset of symptoms, the severity of cyanosis, and the
degree of right ventricular hypertrophy(2). So Fallot is
described in three types depending on the severity or
extent of the anatomical defects(5):

1. Extreme Fallot: F4 + sever pulmonary (atresia

or absent).
2. Classic Fallot: F4 + pulmonary stenosis. Figure 4: Pathophysiology of TOF
3. Pink (acyanotic) Fallot: F4 + mild pulmonary stenosis.

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 December 6, 2009 [TETRALOGY OF FALLOT]

Figure 5 : Blood flow in normal heart and

heart with tetralogy of Fallot

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 December 6, 2009 [TETRALOGY OF FALLOT]

Clinical picture:
A. Symptoms:

1. Cyanosis:(5)
 Onset of cyanosis usually observed weeks after delivery when the ductus
begins to close as PDA in the early postnatal life redirect a large portion of
partially oxygenated blood leaving the heart for the body to the lungs
increasing flow through the pulmonary circulation with relatively better
oxygenation.
 Or sever cyanosis at birth in infant with TOF associated with pulmonary
atresia.

2. Paroxysmal hypercyanotic attacks (hypoxic, “blue,” or “tet” spells)(2)(3)(figure 6):

are particular problems during the 1st 2 yr of life, with a peak
incidence between 2 and 4 months of age. Hypoxic spells
are characterized by a paroxysm of hyperpnoea (i.e., rapid
and deep respiration), irritability and prolonged crying, chest
infection, increasing cyanosis, and decreasing intensity of
the heart murmur as flow across the right ventricular outflow
tract diminishes. These spells usually occur in the morning
after crying, feeding, or defecation. The onset is usually
spontaneous and unpredictable. The spells may last from a
few minutes to a few hours but are rarely fatal. A severe spell Figure 6 : hypoxic spells
may lead to limpness, convulsion, cerebrovascular accident,
and may progress to unconsciousness and, occasionally, to
hemiparesis. Infants who are only mildly cyanotic at rest are often more prone to
the development of hypoxic spells because they have not acquired the
homeostatic mechanisms to tolerate rapid lowering of arterial oxygen saturation,
such as polycythemia.

3. Dyspnea occurs on exertion(2). Characteristically, children assume a squatting

position for the relief of dyspnea caused by physical effort; the child is usually able
to resume physical activity within a few minutes. These findings occur most often in
patients with significant cyanosis at rest.
4. Low birth weight.(5)
5. Poor feeding, breathlessness and agitation.(5)
6. Growth and development may be delayed in patients with severe untreated
tetralogy of Fallot, particularly when oxygen saturation is chronically <70%. Puberty
may also be delayed in patients who do not undergo surgery.(2)
7. TB infection due to decrease pulmonary blood flow.

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 December 6, 2009 [TETRALOGY OF FALLOT]

B. Signs:

-Delayed central cyanosis.

It is most prominent in the mucous membranes of the lips

and mouth and in the fingernails and toenails. neonatal
cyanosis is noted immediately in severe degrees of
pulmonary stenosis.

older children with long standing cyanosis who have not

undergone surgery may have dusky blue skin, grey sclera
with engorged blood vessels and marked clubbing of Figure 7 : cyanotic signs
fingers and toes.(2)(figure 7)

Infants with acyanotic Tetralogy of Fallot may be asymptomatic or may show signs of
CHF from a large right-to-left ventricular shunt.(3)

-Children assume a squatting position for the relief of dyspnea caused by physical effort;
the child is usually able to resume physical activity within a few minutes.(2)
Squatting increases the pressure transiently in the aorta and left ventricle, causing less
blood to move into the left ventricle, more out the pulmonary artery to the lungs.(9)

-The pulse is usually normal, as is venous and arterial pressure.

-By inspection:
 The apex is shifted outwards and diffuse in extent.
 The left anterior hemithorax may bulge anteriorly because of right
ventricular hypertrophy.
 There are parasternal pulsations.

- Palpation reveals:
 Right ventricular predominance.
 In about half the cases, a systolic thrill is felt along the left sternal border in
the 3rd and 4th parasternal spaces.
 A left parasternal heave can be detected.
 A thrill may be felt in the pulmonary area.
 No special character and no thrills are felt on the apex.

-On percussion: Increased area of cardiac dullness on both sides of the chest.

-On auscultation:
 The first heart sound (S1) is normal.
 The second heart sound (S2) is single.

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 December 6, 2009 [TETRALOGY OF FALLOT]

 A systolic murmur is usually loud (grade 3 to 5/6) and harsh; it may be

transmitted widely, especially to the lungs, but is most intense at the left
sternal border. The murmur is generally ejection in quality. It may be
preceded by a click. It is caused by turbulence through the right
ventricular outflow tract. (2)

The more severe the obstruction of the right ventricular outflow tract, the
shorter and softer the systolic murmur. In a deeply cyanotic neonate with
Tetralogy of fallot with pulmonary atresia, heart murmur is either absent or
very soft, although a continuous murmur representing PDA may be
occasionally audible.(3)

Investigations:

Chest Radiography: (figure 8)

There is a normal-sized boot-shaped heart (coeur en sabot) with prominence of the right
ventricle, elevation of the apex and a concavity in the region of the underdeveloped
right ventricular outflow tract and main pulmonary artery. The pulmonary vascular
markings are typically diminished.(4)

Figure 8: coeur en sabot

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 December 6, 2009 [TETRALOGY OF FALLOT]

Electrocardiogram (ECG):
Figure 10 : tall-peaked-bifid
P wave

peaked

bifid

Figure 9 : ECG of right ventricular hypertrophy

ECG demonstrates right axis deviation and evidence of right ventricular hypertrophy.
Note the tall R waves in the right precordium and deep S waves in V6.The positive T
waves in V4R and V1are also characteristic of right ventricular hypertrophy. (figure 9)
P wave is tall and peaked or sometimes bifid .(figure 10)

Echocardiography: (figure 11)

- echocardiography establishes the diagnosis and

provides information about the extent of aortic
override of the septum, the location and degree of
the right ventricular outflow tract obstruction, the
associated ventricular septal defect, the size of the
proximaI branch pulmonary arteries, and the side of
the aortic arch. The Echocardiogram is also useful in
determining whether a PDA is supplying a portion of
the pulmonary blood flow. (2)

Figure 11: TOF echo

Cardiac catheterization:

a catheter is inserted through the skin into a blood vessel (usually in the groin)
and advanced up the inferior vena cava into the heart. An x-ray image is taken while a
small amount of dye is infused. The dye helps highlight the ventricular septal defect,
pulmonary stenosis, overriding aorta, and the size of the pulmonary arteries.(9)

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Lab tests:

Polycythemia as the body attempts to compensate for the lack of oxygen to the
tissues.

MRI:

The goals of MRI after tetralogy of Fallot repair include the quantitative assessment of left
and particularly right ventricular volumes, stroke volumes and ejection fraction; imaging
of the anatomy of the right ventricular outflow tract, the pulmonary arteries, the aorta
and aortopulmonary collaterals; and quantifying pulmonary, aortic, and tricuspid
regurgitation. (4)

Complications:(2)(9)
 Bacterial endocarditis may occur in the right ventricular infundibulum or on
the pulmonic, aortic, or, rarely, tricuspid valves. Endocarditis may complicate
palliative shunts or, in patients with corrective surgery, any residual pulmonic
stenosis or VSD.
 Arrythmia: junctional tachycardia
 Heart block:postoperative due to right bundle branch block after right
venriculotomy Pulmonary valve regurge with right ventricular
enlargement[postoperative]

 Cerebral thrombosis, usually occurring in the cerebral veins or dural sinuses

and occasionally in the cerebral arteries, are common in the presence of
extreme polycythemia and dehydration. Thromboses occur most often in
patients younger than 2 yr. These patients may have iron deficiency anemia,
frequently with hemoglobin and hematocrit levels in the normal range (but
too low for cyanotic heart disease).

 Brain abscess is less common than cerebral vascular events and extremely
rare when most patients are repaired at young ages. Patients with a brain
abscess are usually older than 2 yr. The onset of the illness is often insidious
and consists of low-grade fever or a gradual change in behavior, or both.
Some patients have an acute onset of symptoms that may develop after a
recent history of headache, nausea, and vomiting. Seizures may occur;
localized neurologic signs depend on the site and size of the abscess and the
presence of increased intracranial pressure.

 Heart failure is not a usual feature in patients with the tetralogy of Fallot. It
may occur in a young infant with “pink” or acyanotic tetralogy of Fallot. As
the degree of pulmonary obstruction worsens with age, the symptoms of
heart failure resolve and eventually the patient experiences cyanosis, often
by 6–12 mo of age.

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 December 6, 2009 [TETRALOGY OF FALLOT]

 Delayed growth and development

 Death due to:

1. Prolonged, severe hypoxia which may lead to shock,respiratory failure

and acidosis
2. Arrythmia
3. Heart failure

Medical treatment of fallot tetralogy: (2)(10)(11)(12)

Once tetralogy of Fallot is diagnosed, the immediate management focuses on

determining whether the child's oxygen levels are in a safe range.
1. prostaglandin E1:
dose: (0.01–0.20 μg/kg/min]
route:iv infusion
mechanism :
(a potent and specific relaxant of ductal smooth muscle
is usually initiated to keep the ductus arteriosus open which will provide additional
pulmonary blood flow and increase the child's oxygen level.

This is continued through the preoperative period and during cardiac

catheterization.
2. Treatment of arrythemia[junctional tachycardia] by temporary pacemaker and ,
prophylactic antiarrhythmic therapy
3. Heart block treated by placement of a permanently implanted pacemaker
4. Treatment of cyanotic spells:
 Put the patient in squatting position
 Oxygen for correction of anoxia
 NAHCO3(1-2meq/kg)
 Inderal iv [0.1-0.2mg /kg]to relax infandibualr spasm
 Morphione[0.2mg/kg]in resistant cases
 . Oral propranolol (0.5–1 mg/kg every 6 hr)
5. iron therapy : decrease frequency of Paroxysmal dyspneic attacks
and increases RBCs count so it improve exercise tolerance and general well-being
6. prophylaxis against bacterial endocarditis:
Antibiotic prophylaxis is essential before and after dental and certain surgical
procedures associated with a high incidence of bacteremia. .

7. Prevention or treatment of dehydration is important to avoid hemoconcentration

and possible thrombotic episodes.
8. Treatment of heart failure : digoxin and diuretics
9. Lifestyle and home remedies:(13)

 give baby smaller more frequent meals

 Remain calm if your baby has a cyanotic spell. This will reduce your child's
anxiety
 Good oral hygiene
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 Exercising and play:after surgery patient may participate in normal

activities and avoid competitive sports

Surgical treatment of TOF:(2)(14)(15)

Treatment of the tetralogy of fallot depends on the severity of the right ventricular
outflow tract obstruction. Infants with sever tetralogy requiremedical treatment and
surgical intervention in the neonatal period. Therapy is aimed at providing an immediate
increase in pulmonary blood flow to prevent the sequalae of severe hypoxia. Prolonged,
sever hypoxia may lead to shock, respiratory failure and acidosis and will significantly
reduce the chance of survival, even when surgically amenable lesions are present. Cold
increases oxygen consumption, which places additional stress on a cyanotic infant,
whose oxygen delivery is already limited. Blood glocuse level should be monitored
because hypoglycemia is more likely to develop in infants with cyanotic heart diseases.
Infants with symptoms and sever cyanosis in the 1st month of life have marked obstruction
of the right ventricular outflow tract or pulmonary atresia.

Two options are available:

1- Palliative systemic to pulmonary artery shunt:
Aim: to augment pulmonary artery blood flow, to:
A) decease the amount of hypoxia
B) improve linear growth
C) Augment growth of the branch pulmonary arteries
.
Indications

Shunt procedures are performed to increase PBF. Indications for shunt procedures vary
from institution to institution. Many institutions, however, prefer primary repair without a
shunt operation regardless of the patient's age. However, when the following situations
are present, a shunt operation may usually be chosen rather than primary repair.

1. Neonates with TOF and pulmonary atresia

2. Infants with hypoplastic pulmonary annulus, which requires a transannular patch
for complete repair
3. Children with hypoplastic PAs
4. Unfavorable coronary artery anatomy
5. Infants younger than 3 to 4 months old who have medically unmanageable
hypoxic spells
6. Infants weighing less than 2.5 kg

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 December 6, 2009 [TETRALOGY OF FALLOT]

Technique:
Although several other procedures were performed in the past (see Fig. 14-22 ), a
modified Blalock-Taussig (Gore-Tex interposition) shunt is the only popular procedure
performed at this time. Occasionally, a classic Blalock-Taussig shunt is performed.
1. Classic Blalock-Taussig shunt, anastomosed between the subclavian artery and
the ipsilateral PA, is usually performed for infants older than 3 months (see Fig. 14-
22 ) because the shunt is often thrombosed in younger infants with smaller
arteries. A right-sided shunt is performed in patients with left aortic arch; a left-
sided shunt is performed for right aortic arch.
2. Modified Blalock-Taussig (BT) shunt. A Gore-Tex interposition shunt is placed
between the subclavian artery and the ipsilateral PA. This is the most popular
procedure for any age, especially for small infants younger than 3 months of age
(see Fig. 14-22 ). A left-sided shunt is preferred for patients with a left aortic arch,
whereas a right-sided shunt is preferred for patients with a right aortic arch. The
surgical mortality rate is 1% or less.
3. The Waterston shunt, anastomosed between the ascending aorta and the right
PA, is no longer performed because of a high incidence of surgical complications
(see Fig. 14-22 ). Complications resulting from this procedure included too large a
shunt leading to CHF or pulmonary hypertension, of both, and narrowing and
kinking of the right PA at the site of the anastomosis. This created difficult
problems in closing the shunt and reconstructing the right PA at the time of
corrective surgery.
4. The Potts operation, anastomosed between the descending aorta and the left
PA, is no longer performed either (see Fig. 14-22 ). It may result in heart failure or
pulmonary hypertension, as in the Waterston operation. A separate incision (i.e.,
left thoracotomy) is required to close the shunt during corrective surgery, which is
performed through a midsternal incision.

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 December 6, 2009 [TETRALOGY OF FALLOT]

Complications:
1) Chylothorax: treated by repeated thoracocentesis or reoperation the ligate the
thoracic duct.
2) Diaphragmatic paralysis: requires prolonged ventilator support and vigorous
physical therapy, until the function of the phrenic nerve returns in 1 to 2 months(
unless it's completely devided )
3) Horner syndrome: usually temporary and doesn't require treatment.

Successful shunt procedure will result in disappearance of the cyanosis. The

development of a continuous murmur over the lung fields after
the operation indicates a functioning anastomosis. A good continuous
shunt murmur may not be heard until several days after
surgery.

The duration of symptomatic relief is variable. As the child

grows, more pulmonary blood flow is needed and the shunt
eventually becomes inadequate.
When increasing cyanosis develops, a corrective operation
should be performed if the anatomy is favorable. If not
possible (because of hypoplastic branch pulmonary
arteries) or if the 1st shunt lasts only a brief period in a small
infant, a second aortopulmonary anastomosis may be
required on the opposite side.

2- Corrective surgical therapy ( complete intracardiac repair) :

a) Ventricular hypertrophy: Removing obstructive muscle bunbles in the right

ventricle to relief the right ventricular outflow tract obstruction.
b) Patch closure of the VSD
c) Pulmonary stenosis: Vulvotomy if the pulmonary
valve is stenotic.
Vulvectomy if the pulmonary valve annulus is
extremely thickened.

(figure 12: Complete surgical correction for tetralogy of

Fallot. Sketch of corrective surgery for tetralogy of Fallot.
Diagram shows closing of ventricular septal defect and
widening of right ventricular outflow tract with patching of
infundibular tract (gray).)

NB: Any previously established shunt MUST be ligated and

divided before full repair.

Figure 12

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 December 6, 2009 [TETRALOGY OF FALLOT]

Prognosis:
After successful total correction, patients are generally asymptomatic and are able to
lead unrestricted lives.

Immediate post operative complications:

1) right ventricular failure: treated by diuretics and positive inoropic agent
2) transient heart block
3) residual VSD with left to right shunting
4) myocardial infarction from interruptionof an aberrant coronary artery.
5) Pulmonary incompetence: if severe, it requires reoperation.

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 December 6, 2009 [TETRALOGY OF FALLOT]

References

Textbook:
th
1) Medical Embryology 9 edition page 250

2) Nelson Textbook of Pediatrics,18 ed, chapter 430 ( Cyanotic congenital heart lesions:
Lesions Associated with decreased pulmonary blood flow, tetralogy of fallot)

3) Tetralogy of Fallot.Park textbook: Pediatric Cardiology for Practitioners, Elsevier ,5th ed.

4) Zipes:Tetralogy of Fallot. Braunwald's Heart Disease: A Textbook of Cardiovascular

Medicine, Elsevier,7th ed.

5) Fundamentals of pediatrics, Third edition 2008 ,Faculty of medicine, Ain Shams

university.

6) www.wikipedia.com

7) www.nlm.nih.gov/medlineplus/ency/article/001567.htm

8) www.whonamedit.com/synd.cfm/2280.html

9) www.emedicine.com

10) www.pubmed.gov.com

11) www.mayoclinic.com

12) www.medlineplus.com

13) www.american heart .com

14) www.ajronline.org/cgi/content-nw/full/189/6/1353/FIG24

15) www.pediatriconcall.com/FORDOCTOR/Diseasesand

[Department of pediatrics] | Prof. Mona El-Samahy unit 17

‫‪December 6, 2009‬‬ ‫]‪[TETRALOGY OF FALLOT‬‬

‫‪Teamwork‬‬

‫كرين هحود حٌفي هحود (‪)798‬‬

‫كرين ًاجي هحود عبد الحلين (‪)801‬‬

‫كرين يضرى هجلي كيرلش (‪)802‬‬

‫كوثر صيد هعوض عبد الحويد (‪)803‬‬

‫كيرلش جرجش تقاوى قلدس (‪)804‬‬

‫كيرلش رأفت عصام القوص صوعاى فيلبش (‪)805‬‬

‫كيرلش صوير هٌرى صادق (‪)806‬‬

‫الرا أشرف جالل اصواعيل (‪)808‬‬

‫لبٌي عبد الفتاح هحود حضي (‪)811‬‬

‫لبٌي عز الديي هحود فودة (‪)812‬‬

‫‪[Department of pediatrics] | Prof. Mona El-Samahy unit‬‬ ‫‪18‬‬