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VENTRICULAR SEPTAL DEFECT VSD

1- Embryology. 2- Anatomy. 3- HEMODYNAMICS. 4- Sings & Symptoms. 5- Natural History. 6- Investigations( X-ray & ECG ) 7- Investigations( Catheterization &EchoCardiology) 8- Treatment( Transcatheterization &Surgery)

Embryology
At 4-8 weeks' gestation, the single ventricular chamber is effectively divided into 2. This division is accomplished with the fusion of the membranous portion of the ventricular septum, the endocardial cushions, and the bulbous cordis (proximal portion of the truncus arteriosus). The muscular portion of the ventricular septum grows cephalad as each ventricular chamber enlarges, eventually meeting with the right and left ridges of the bulbous cordis. The right ridge fuses with the tricuspid valve and the endocardial cushions, separating the pulmonary valve from the tricuspid valve. The left ridge fuses with a ridge of the interventricular septum, leaving the aortic ring in continuity with the mitral ring. The endocardial cushions develop concomitantly and finally fuse with the bulbar ridges and the muscular portion of the septum. The fibrous tissue of the membranous portion of the interventricular septum makes the final closure and separates the 2 ventricles.

Anatomy
The interventricular septum is a curvilinear complex structure and can be divided into 4 zones by anatomic landmarks in the right ventricle (RV) as shown in the image below. The RV has many heavy trabeculations. The stoutest of these is a Y -shaped bundle (ie, the trabecula septomarginalis), which proceeds toward the apex and which gives rise to the moderator band that courses transversely near the apex. The trabecula septomarginalis is an important structure that helps in the identification of the RV, regardless of its location in the chest. The 2 limbs of the Y travel superiorly, and the anterior, or parietal, limb supports the pulmonic valve and the posterior limb (septal band)

extends to the membranous septum. The 4 parts of the ventricular septum are as follows: 1. the inlet septum is smooth walled and extends from the septal attachments of the tricuspid valve to the distal attachments of the tricuspid tensor apparatus. This region has also been called the AV canal septum.4 2. The apical trabecular zone separates the coarse trabeculations of the RV from the fine ones seen in the left ventricle (LV). Van Praagh et al refer to this as the muscular septum or the ventricular sinus septum.4 3. The smooth-walled outlet or infundibular septum is separated from the trabeculated portion of the RV by the septal band of the trabecula marginalis. Van Praagh et al called this area the parietal band or the distal conal septum and refer to defects in this area as conal septal defects.4 4. The last and the smallest region in the ventricular septum is the membranous septum. This lies between the anterior and the septal tricuspid leaflets and below the right and the noncoronary cusps of the aortic valve. o The 3 muscular components of the ventricular septum described above abut on the membranous septum and fan out from it as triangles, with the apices touching this septum. In the normal heart, the tricuspid and mitral valves are attached to the ventricular septum at different levels so that the tricuspid-valve attachment is apically displaced compared with the mitral-valve attachment. Therefore, a portion of the interventricular septum, called the AV septum, lies between the right atrium (RA) and the LV. This portion consists of a membranous part anteriorly and a muscular part posteriorly and is usually present in most hearts with an isolated ventricular septal defect. o In the anterior aspect, the tricuspid-valve attachment divides the area of membranous septum into an interventricular component (between the LV and RV) and an AV component (between the LV and RA). When a ventricular septal defect is isolated, the AV component of membranous septum is usually intact.

Anatomy&Types
Ventricular septal defects (VSDs) are classified by the position they occupy in the ventricular septum.

The septum is divided into 4 components: 1-the membranous septum, 2-the inlet. 3-the trabecular. 4- the outlet parts of the muscular septum. (The outlet septum is also called the conal or infundibular septum.) Thus, 4 anatomic types of VSDs exist.

Type I defects(subarterial-conal-outlet): *are also known as: subarterial, outlet, or conal defects.

*These defects comprise 5% of all VSDs and are located in the outlet portions of the left and right ventricles. *The superior edge of the VSD is the conjoined annulus of the aortic and pulmonary valves. *Because the aortic and pulmonary valves are in fibrous continuity, this type of defect may also be referred to as doubly committed subarterial. *(They are also called juxta-arterial, supracristal, subpulmonary, infundibular, or conoseptal defects.) *This VSD is associated with prolapse of the unsupported aortic valve cusps and progressive aortic regurgitation.

Type II defects (infracristal-subaortic-perimembranous): * They are also called infracristal, subaortic, perimembranous, or paramembranous defects. *These defects are the most common type of VSD, comprising 75% of all VSDs. * They occur around the membranous septum and the fibrous trigone of the heart and are associated with a muscular defect at a portion of their perimeter. *The defect is near the aortic valve, and the annulus of the tricuspid valve contributes to the rim of the defect. *Perimembranous defects are divided into 3 major subtypes according to the adjacent portion of the muscular septum:

1-perimembranous inlet 2- perimembranous trabecular 3- perimembranous outlet.

Type III defects (atrioventricular canal-AV septal-inlet septal): *also called atrioventricular (AV) canal, AV septal, or inlet septal defects, *(10% of all VSDs). * are located in the posterior region of the septum beneath the septal leaflet of the tricuspid valve.

Type IV defects (Muscular):

*also called muscular defects, have entirely muscular rims. *(10% of all VSDs). *They may be single but are commonly multiple *Muscular defects may be divided into several categories: inlet, trabecular, central, apical, marginal, and outlet (infundibular). * Most commonly, multiple defects occur in the apical trabecular septum. * In its most severe form, multiple defects of the ventricular septum are sometimes descriptively referred to as Swiss cheese septum.

HEMODYNAMICS
The physical size of the VSD is a major,but not the only determinant of the size of the left-to-right shunt. The level of pulmonary vascular resistance in relation to systemic vascular resistance also determines the shunt's magnitude. When a small communication is present (usually < 0.5 mm2), the VSD is called restrictive and right ventricular pressure is normal. The higher pressure in the left ventricle drives the shunt left to right; the size of the defect limits the magnitude of the shunt. In large nonrestrictive VSDs (usually >1.0 cm2), right and left ventricular pressure is equalized. In these defects, the direction of shunting and shunt magnitude are determined by the ratio of pulmonary to systemic vascular resistance. After birth in patients with a large VSD, pulmonary vascular resistance may remain higher than normal, and thus the size of the left-to-right shunt may initially be limited. As pulmonary vascular resistance continues to fall in the 1st few weeks after birth because of normal involution of the media of small pulmonary arterioles, the size of the left-to-right shunt increases. Eventually, a large left-to-right shunt develops, and clinical symptoms become apparent. In most cases during early infancy, pulmonary vascular resistance is only slightly elevated, and the major contribution to pulmonary hypertension is the extremely large pulmonary blood flow. In some infants with a large VSD pulmonary arteriolar medial thickness never decreases. With continued exposure of the pulmonary vascular bed to high systolic pressure and high flow, pulmonary vascular obstructive disease develops. When the ratio of pulmonary to systemic resistance approaches 0 .5 : 1, the shunt becomes bidirectional the patient becomes cyanotic (Eisenmenger syndrome).

Clinical Picture of VSD :

Small sized VSD : Symptoms : Patients have mild or no symptoms. These cases are most often brought to the cardiologist's attention because a murmur is detected during routine examination. o Feeding or weight gain is usually not affected ( Normal thriving )
o o

Signs :
o o o

Patients may have normal vital signs. Physiologic splitting of S2 is usually retained. The characteristic harsh, holosystolic murmur is loudest along the lower left sternal border (LSB), and it is well localized. Small defects can produce a high-pitched or squeaky noise. The murmur is usually detected after the PVR decreases at about 4-8 weeks of age.

Medium sized VSD: Symptoms:


o o o

o o o

Babies may have excessive sweating due to increased sympathetic tone. This sweating is especially notable during feeds. An important symptom is fatigue with feeding. A sensitive symptom may be the lack of adequate growth (unable to thrive), which is due to and an inability of the infant to feed adequately and decrease systemic blood flow . Frequent respiratory infections may occur secondary to the plethoric lungs. Symptoms, which begin as pulmonary vascular resistance (PVR) decreases, may be clearly apparent by age 2-3 months. Symptoms occur earlier in the premature infant than in the full-term infant because pulmonary resistance decreases earlier in preterm babies than in term babies.

Signs:
o o o o

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Infants often have a normal length and decreased weight. Poor weight gain is a sensitive indicator of congestive heart failure (CHF). Infants may have mild dyspnea and tachypnea due to plethoric lungs . Tachycardia ,gallop rhythm, tachypnea , and enlarged liver which indicate heart failure . The murmur with moderate-sized defects is usually associated with thrill. A holosystolic harsh murmur is most prominent over the lower LSB. The intensity of the pulmonary component is usually normal or slightly increased. In addition to the harsh holosystolic murmur, a diastolic rumble may be detected in the mitral area. This rumble suggests functional mitral stenosis secondary to a large left-to-right shunt qhich leads to increase blood flow to the left atrium .

Large sized VSD: Symptoms: Symptoms are similar to symptoms with moderate defects. , but more severe. o Symptoms may be delayed, as they are with large defects, because of a delayed decrease in pulmonary vascular pressures. o Poor weight gain and frequent respiratory infections are common.
o

Signs:
o o

The same signs of moderate defect . Signs of CHF are present. The cardinal signs of heart failure include tachycardia , gallop rhythm, tachypnea, and hepatomegaly. In addition, cardiomegaly is present . The murmur is pansystolic but poorly localized and is usually associated with a diastolic rumble.

Eisenmenger syndrome: Symptoms:


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At rest, patients may have no symptoms With exercise, symptoms include exertional dyspnea, cyanosis, chest pain, syncope, and hemoptysis.

Signs:
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Children with Eisenmenger syndrome may have tachypnea only with exercise and not at rest. They may be only mildly cyanotic at rest but then develop profound cyanosis with exercise.

Natural history:
Small VSD: One-third to one-half of all small VSDs close spontaneously (on their own). This seemingly miraculous event occurs most often before the baby is 1 year old, almost always before age 4 (75% by 2 years of age). Closure may occur by means of hypertrophy of the septum, formation of fibrous tissue, subaortic tags, apposition of the septal leaflet of tricuspid valve, or (in rare cases) prolapse of a leaflet of the aortic valve. When perimembranous ventricular septal defects close because of development of fibrous tissue or the apposition of the tricuspid valve, an aneurysm of the interventricular septum may appear. Even if a small VSD does not close spontaneously, surgical repair is usually not recommended. However, long-term follow-up is required.

Moderate (or medium-sized) VSDs are less likely than small defects to close on their own. They may require surgery to close and may cause symptoms during infancy and childhood. Large VSD : With a large VSD (usually one greater than 1 cm2), there is significant shunting of blood from the left ventricle into the right ventricle. Thus extra blood volume puts a strain on the right ventricle and causes an increase in the blood pressure of the lungs called "pulmonary hypertension." The child may have labored breathing, difficulty feeding, grow poorly, and have pallor. Complications: A small ventricular septal defect may never cause any problems. Larger defects can cause a wide range of disabilities from mild to life-threatening. Treatment can prevent many of these complications. Eisenmenger's syndrome: Ultimately, if a large ventricular septal defect goes untreated, increased blood flow to the lungs causes high blood pressure in the lung arteries (pulmonary hypertension). Over time, permanent damage to the lung arteries develops and the pulmonary hypertension can become irreversible. This complication, called Eisenmenger's syndrome, may occur in early childhood, or it can develop slowly over many years. In people with Eisenmenger's syndrome, the majority of the blood flow through the ventricular septal defect goes from the right ventricle to the left and bypasses the lungs. This means deoxygenated blood is pumped to the body and leads to a bluish discoloration of the lips, fingers and toes (cyanosis) and other complications. Once a person has Eisenmenger's syndrome, it's too late to surgically repair the hole because irreversible damage to the lung arteries has already occurred. Signs and Symptoms of Eisenmenger's syndrome
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Signs and symptoms of Eisenmenger's syndrome include: Gallstones Cyanosis, a blue tinge to the skin resulting from lack of oxygen. High red blood cell count Swollen or clubbed finger tips(clubbing) Fainting, called syncope Heart failure Arrhythmia or irregular heart rhythms Bleeding disorders Coughing up blood Iron deficiency Kidney problems Stroke

Other complications may include:




 

Heart failure. The increased blood flow through the heart due to a ventricular septal defect can also lead to heart failure, a chronic condition in which the heart can't pump effectively. Endocarditis. People with a ventricular septal defect are at increased risk of an infection of the heart (endocarditis). Stroke . People with large defects, especially occurring with Eisenmenger's syndrome, are at risk of a stroke due to a blood clot passing through the hole in the heart and going to the brain. Other heart problems. Ventricular septal defects can also lead to abnormal heart rhythms and valve problems.

X-ray and ECG of VSD:


1-In patients with small VSDs, the chest radiograph is usually normal, although minimal cardiomegaly and a borderline increase in pulmonary vasculature may be observed. The electrocardiogram is generally normal but may suggest left ventricular hypertrophy. The presence of right ventricular hypertrophy is a warning that the defect is not small and that the patient has pulmonary hypertension or an associated lesion such as pulmonic stenosis. 2- In large VSDs, the chest radiograph shows gross cardiomegaly with prominence of both ventricles, the left atrium, and the pulmonary artery Pulmonary vascular markings are increased, and frank pulmonary edema, including pleural effusions, may be present. The electrocardiogram shows biventricular hypertrophy; P waves may be notched or peaked.

Echocardiography
Cross sectional echocardiographic examination is now recognised as the technique of choice for diagnosis. Not only does the technique show the presence of a defect, it also permits its accurate localisation. Furthermore, because the defect should be identified in more than one plane, its size can be estimated. Perimembranous defects are recognized in long-axis, fourchamber and short-axis views, with fibrous continuity between the leaflets of the tricuspid and mitral or aortic valves being the pathognomic feature. Perimembranous defects opening to the inlet of the right ventricle are recognised by cuts through the ventricular inlets The four-chamber sections will demonstrate continuity between the leaflets of the tricuspid to mitral valves via the central fibrous body, with loss of the usual off-setting of the hingepoints of the leaflets. A gentle sweep of the transducer from a fourchamber cut to a long axis cut will demonstrate the continuity of the leaflets of the tricuspid and aortic valves through the central fibrous body. In the so-called juxta-tricuspid and non-perimembranous defect, the defect is described as being at some distance from the aortic valve because it does not reach the central fibrous body. We initially believed that we had identified such a defect echocardiographically. When the surgeon closed the defect, however, he discovered a muscular ridge separating the hinges of the tricuspid and mitral valves in the roof of the defect. Hence, the defect was surrounded by muscle, and opened to the inlet of the right ventricle in other words a muscular inlet defect. It remains the fact, therefore, that we have still to identify a patient with a juxta-tricuspid and non-perimembranous defect, either in the clinical setting or at autopsy. Defects opening between the outlets are best identified in the subcostal right oblique section, which shows the muscular outlet septum as an interventricular structure immediately beneath the subpulmonary infundibulum. ( This is evidence of the biventricular aortic connection). The parasternal short-axis cut at the level of the aortic valve will similarly show this discrete outlet septum). When this feature is present, the parasternal long-axis section will usually demonstrate overriding of the leaflets of the aortic valve For those defects opening between the outlets, and associated with posterior longitudinal deviation of the outlet septum, usually in the setting of aortic coarctation or interruption, the parasternal long-axis section will be the optimal plane for diagnosis. Muscular defects opening to the right ventricular inlet are best seen in the four-chamber view, but retain the feature of atrioventricular valvar off-setting. Large defects within the apical trabecular septum are identified in four-chamber and short-axis planes, while muscular defects opening to the subpulmonary outlet are identified in shortaxis or right anterior oblique planes from parasternal or subcostal approaches. The best view with which to distinguish perimembranous from muscular outlet

defects is the high-parasternal short-axis section. This cut demonstrates the presence or absence of continuity between the leaflets of the tricuspid and aortic valves. Small or multiple muscular defects in the apical Muscular septum are those least likely to be visualized without the aid of colour flow mapping. Doubly committed juxta-arterial defects are recognised because of the continuity of the leaflets of the aortic and pulmonary valves in the roof of the defect, with absence of much of the subpulmonary outlet are identified in shortaxis or right anterior oblique planes from parasternal or subcostal approaches. LA LV D RThese features are seen in long-axis , short-axis, and subcostal right oblique views. If present, prolapse of the aortic valvar leaflets will be visualised; see also and. By rotating the transducer to focus on the leaflets of the tricuspid valve, it is also possible to show whether a doubly committed juxta-arterial defect is perimembranous, or is separated from the central fibrous body by a muscular rim. This feature will best be appreciated from the parasternal shortaxis section across the aortic valve. Cross sectional echocardiography also demonstrates the proximity of the defect to structures that may close it, such as aneurysmal formation of tricuspid tissue tags, or plastering of the tricuspid valvar leaflet tissue across the defect. Although transoesophageal echocardiography is not usually necessary in the delineation of ventricular septal defect in childhood, it may provide crucial information when there is straddling or overriding of the tricuspid valve. Identification of the site of the ventricular septal defect at initial examination will also provide hard evidence on the rate of spontaneous closure for different types of defects in different sites. In addition to these specific diagnostic findings, the echocardiogram also reflects the haemodynamic state. Left atrial and left ventricular dilation are easily seen in infants with a high pulmonary blood flow, the left ventricle being hyperdynamic. With large unrestrictive defects, there will be a concomitant increase in right ventricular dimensions, while in small restrictive defects the ventricular size and performance may be normal. Further insight into the physiological state is obtained by studying the motion of the leaflets of the pulmonary valve. With high flow to the lungs, but low pulmonary vascular resistance, the motion is normal. When there is a high pulmonary vascular resistance, the closure line of the leaflets is flattened, and the a-dip disappears. The onset of aortic regurgitation is indicated by the appearance of diastolic vibration of the mitral valve, well appreciated in earlier times on the M-mode tracing, but now visualised directly with colour flow mapping. In this case, the cross sectional echocardiogram should show the abnormalities of the aortic valve responsible for the regurgitation. For example, a prolapsing aortic valvar leaflet may be demonstrated. Alternatively, perforations and vegetations associated with infective endocarditis may be identified. As might be expected, all the advantages of cross sectional echocardiography in diagnosis are accentuated when enhanced by three-dimensional

reconstruction. Such techniques, while not yet generally available, have immense potential, as shown by the reports describing their value.

Doppler Interrogation
The complete evaluation of a ventricular septal defect includes not only an assessment of the size, site and number of defects, but also an estimate of the haemodynamic consequences. By using continuous wave Doppler ultrasound, it is possible to measure the velocity of flow across any ventricular septal defect. Then, by invoking the principles of the Bernoulli equation, it is possible to calculate the instantaneous peak systolic pressure drop between the ventricles. Assuming that the left ventricular peak systolic pressure is the same as the systolic blood pressure, the right ventricular systolic pressure can then be estimated. In the absence of any obstruction within the right ventricular outflow tract, this can be presumed to be equal to the pulmonary arterial systolic pressure. Infants and children with congenital cardiac defects, including those with a ventricular septal defect, frequently have mild tricuspid insufficiency. In this situation, it is possible to estimate the pressure dropacross the tricuspid valve and, therefore, to estimate the right ventricular and pulmonary arterial systolic pressures. A potential source of error arises when there is a shunt from left ventricle to right atrium through the defect via a deficiency in the septal leaflet of the tricuspid valve. In this situation, the regurgitant jet reflects the pressure drop between the left ventricle and right atrium. Colour flow mapping has greatly facilitated the echocardiographic diagnosis of ventricular septal defect. Its most important uses include accurate alignment of the Doppler beam with the flow of blood, thus enhancing accurate quantification of velocity, the detection of multiple ventricular septal defects, and the demonstration of shunting from left ventricle to right atrium. Colour flow mapping also plays a role in distinguishing innocent murmurs from those caused by very small ventricular septal defects.

Cardiac Catheterisation Prior to the advances made in cross sectional echocardiography, catheterisation was an essential part of the assessment of patients having large restrictive and unrestrictive defects. It made possible the measurement of intracardiac pressures, particularly the pulmonary arterial pressure, along with quantification of the flow of blood to the lungs. This information made it possible to calculate the pulmonary vascular resistance. In addition, the technique provides confirmation of the interventricular location of the defect by the detection of a step-up in saturation of oxygen at ventricular level, or by visualisation of the passage of the catheter from right to left ventricle or to the aorta. If the defect is modified by abnormal attachments of the leafletsnof the tricuspid valve, such that the shunt is from left ventricle to right atrium, then the step-up in saturation of oxygen is detected in the right atrium. This is also found when a ventricular septal defect co-exists with an atrial septal defect, or when there is an atrioventricular septal defect. Cardiac catheterisation provides further information about the associated defects. Passage of the catheter from the pulmonary trunk to the descending aorta, for example, indicates the presence of a communication between these two arteries, usually an arterial duct. The findings at catheterisation reflect the pathophysiology. Unrestrictive defects with a high pulmonary blood flow have similar pressures in right and left ventricles. With an unobstructed right ventricular outflow tract, and a low pulmonary vascular resistance, the pulmonary arterial systolic pressure will be similar to that in the aorta. The diastolic and mean pulmonary arterial pressures will be lower than aortic pressures. In such cases, a high flow to the lungs will be measured oximetrically, or in the past by dye dilution curves. In large but restrictive defects, the right ventricular and pulmonary arterial pressures will be lower than those in the left ventricle and aorta. The main current indication for cardiac catheterisation other than for interventional closure of the defect is to establish, beyond doubt, that patients suspected to have pulmonary vascular disease do have an elevation of pulmonary vascular resistance so great as to render them inoperable. found on cardiac catheterisation. This is best performed in the 45-degree head-up position using antero-posterior and

lateral projections. Left ventricular angiograms can be used for quantitative assessment of left ventricular function. Left ventricular enddiastolic volume is usually increased, and the ejection fraction is normal or increased. These indexes have prognostic significance but rarely, if ever, will the decision whether or not to opt for closure be influenced by these findings. Nowadays, it is rarely necessary to perform invasive studies in infants with ventricular septal defects. All the necessary information required to determine the need for surgical

Treatment of VSD: the treatment of the VSDs first was depending on


the appearance of the symptoms of heart failure or cardiac overload but now with the development of the transcatheterization and non invasive devices beside the surgery, there is no point in leaving a VSD opened ( even if it was small and asymptomatic ). Transcatheter: Technique: The catheter needle is inserted in certain sites ( groin, neck) in the vein or artry. Most commonly inserted in the groin in the femoral artry then the needle goes up in the aorta until reached the left ventricles then it pass through the defect (VSD) then the device is put at the site of the defect then its inflated to close the VSD

Indications: usually there is no need to await the symptoms to accour but the most common indications are: 1-symptoms of heart failure. 2- signs of left heart chambers overload 3- recurrence of endocarditis 4-preventionof pulmonary arterial hypertension, ventricular dysfunction, arrhythmias and aortic regurgitation. 5-its indicated mainly in small VSDs. Contraindications: 1-Severe uncontrolled hypertension 2-Ventricular arrhythmias 3-Acute stroke 4-Severe anemia 5-Active gastrointestinal bleeding 6-Acute renal failure 7-Uncompensated congestive failure (patient cannot lie flat). 8-Unexplained febrile illness and/or untreated active infection. 9-Electrolyte abnormalities (eg, hypokalemia) 10-Severe coagulopathy.. 11- heamoragic disorders. Before any diagnostic or theraputic catheterization the above complications should be managed first to ensure successeful catheterization. Absolute contraindication : 1-aortic stenosis (never try arterial transcatheterization) 2-pulmonary hypertension.(usually requires surgery and no need or benefit from transcatheterization). Complications: 1-malposition or dislocation of the transcatheter device. 2-injury of the femoral artery at the puncture site 3-left ventricular perforation after dislocation of the device. 4- embolization of the device in any vein ( iliac vein device embolization was reported). 5-in some occluder devices over-inflation of the ballons lead to more widening of the defect.

Surgery: its the gold standard in treatment of any septal defects including the VSDs but we should consider it as the last solution because of its high morbidity and mortality besides the patient refusal (most of times). Before any cardiac surgery All imaging studies should be reviewed preoperatively to clearly visualize the defect(s) and to assess for the presence of other intracardiac anomalies. These studies delineate the anatomic substrate and allow appropriate planning for the operation

Technique: Intraoperative Details VSDs are closed through a median sternotomy approach. Cardiopulmonary bypass using dual caval cannulation (inferior vena cava [IVC] and superior vena cava [SVC]) and cardioplegic diastolic arrest provide a bloodless, motionless field for intracardiac closure. Most VSDs may be closed working through an incision in the right atrium (transatrial approach). The surgeon inspects and repairs the VSD looking through the right atrium, across the tricuspid valve, and into the right ventricle. To visualize defects of the inlet septum, detachment of the septal leaflet of the tricuspid valve may be required. Conal VSDs may be approached through an incision in the main pulmonary artery (PA) working across the pulmonary valve (transpulmonary approach). Conal VSDs with associated aortic valve insufficiency may be approached through an incision in the ascending aorta, allowing VSD closure and aortic valve repair (transaortic approach). Muscular VSDs may be approached through the ventricular apex (transventricular approach). Most surgeons close the defect using a synthetic patch (Dacron or polytetrafluoroethylene [PTFE] or a patch from the patient own pericardium) sewn to the rightward aspect of the VSD with a running nonabsorbable monofilament suture. Avoid placing deep sutures in the area of conduction tissue to prevent postoperative heart block. Postoperative Details Most children rapidly recover from VSD closure. Extubation usually occurs in the ICU in the hours following surgery. Children requiring postoperative inotropic support, pressor support, or both are weaned within 24 hours postsurgery. Postoperative diuretic therapy is generally needed to return intravascular volume to normal levels. For the small proportion of children with hemodynamically significant pulmonary hypertension (PA pressure >50-75% of systemic arterial pressure), continued sedation with mechanical ventilation (to maintain normal arterial oxygen and carbon dioxide tensions) and pulmonary vasodilators (eg, nitric oxide, sildenafil) may be used until pulmonary vasculature relaxes within several days after surgery. After closure, the cardiac rhythm should be observed. Temporary cardiac pacing is necessary in children with transient heart block. Most children are transferred from the ICU on the first or second postoperative day. Within 48 hours, mediastinal drainage tubes are removed. Many patients are ready for discharge within 4-7 days of surgery.

Indication: 1-its the gold standard to close any septal defect including VSDs but its recommended in large VSDs or when other non-invasive procedurs . 2-To handle the complication of malpositioned or dislocated patch(ex: complications of transcatheter). 3-multiple cardiac defects ( multiple VSDs).

Complication: 1-infection 2-postoperative bleeding requiring re-exploration 3- valve injury (tricuspid, pulmonary, or aortic) leading to valve regurgetation 4-pulmonary hypertension with poor cardiac output 5-atrioventricular (AV) heart block 6-residual VSD with continued left-to-right shunting 7-death. Permanent AV heart block occurs in 1% or fewer of children undergoing VSD closure. Care must be taken to correctly identify the position of the defect, since this determines the location of conduction tissue and directs the repair to avoid conduction injury. Transient AV block is treated expectantly with temporary cardiac pacing. When AV conduction does not return (in <1% of patients in the best centers), a permanent pacemaker is needed. Residual left-to-right shunt from incomplete VSD closure may result from insufficient intraoperative exposure or suture disruption with patch dehiscence. Significant residual shunting is most commonly observed in muscular defects (particularly multiple defects) in which trabeculations decrease visualization of the full extent of the VSD(s). Residual shunting with Qp:Qs greater than 1.5:1 occurs in 2% or fewer of patients and should prompt reoperation. The mortality rate associated with surgical VSD closure has decreased dramatically with improvements in perfusion, myocardial protection, and postoperative care. The overall surgical mortality rate for patients with isolated VSD is less than 1%, and the mortality rate for low-risk candidates is miniscule. Risk factors for mortality include severe associated noncardiac anomalies, multiple VSDs, and major associated cardiac anomalies.

N.B: before any intervention and trials to close any VSD we should leave adequet time for the VSD to close sponteniously.( as most of VSDs tend to have nature history of closure without any treatment ).