Ventricular Septal Defect in Children - Clinicals, Diagnosis, and Management

Cardiology

Clinicals - History

Fact Explanation
An asymptomatic child, referred following routine clinical examination. In small ventricular septal defects <0.5cm2, the defect is restrictive and right ventricular pressure remains normal. At birth and in the first few weeks following, the pulmonary vascular resistance remains high. As a result, the magnitude of the left to right shunt and the symptoms are minimal. An asymptomatic child, referred following routine clinical examination.
In small ventricular septal defects <0.5cm2, the defect is restrictive and right ventricular pressure remains normal. At birth and in the first few weeks following, the pulmonary vascular resistance remains high. As a result, the magnitude of the left to right shunt and the symptoms are minimal.
A 2-3 months child with excessive sweating (scalp sweating noticed by the mother) with feeding. In moderate to large defects. Sympathetic over-stimulation following heart failure. The symptoms appear few weeks later as the pulmonary vascular resistance decreases with time and the magnitude of the left to right shunt becomes greater. A 2-3 months child with excessive sweating (scalp sweating noticed by the mother) with feeding.
In moderate to large defects. Sympathetic over-stimulation following heart failure. The symptoms appear few weeks later as the pulmonary vascular resistance decreases with time and the magnitude of the left to right shunt becomes greater.
Fatigue during feeding. In moderate to large defects. Feeding increases the cardiac output and sympathetic over-stimulation. It is a feature of heart failure and presents after first few weeks of life. Fatigue during feeding.
In moderate to large defects. Feeding increases the cardiac output and sympathetic over-stimulation. It is a feature of heart failure and presents after first few weeks of life.
Growth faltering, loss of gained weight. In moderate to large defects. It is evident with onset of heart failure and a feature of increased calorie requirement. Growth faltering, loss of gained weight.
In moderate to large defects. It is evident with onset of heart failure and a feature of increased calorie requirement.
Recurrent respiratory tract infections. The left to right shunt increases the pulmonary blood flow, and thus in turn causes vascular congestion in the lungs. This acts as a predisposing factor for recurrent respiratory infections. Recurrent respiratory tract infections.
The left to right shunt increases the pulmonary blood flow, and thus in turn causes vascular congestion in the lungs. This acts as a predisposing factor for recurrent respiratory infections.
More severe forms of weight loss, shortness of breath and respiratory tract infections that presents a few weeks later than above symptoms In large defects. The symptoms are more severe but they occur a few weeks later on than the children with moderate defects. The reason behind this is in larger defects, the pulmonary vascular medial remodeling starts and happens later and slower than those with smaller defects. More severe forms of weight loss, shortness of breath and respiratory tract infections that presents a few weeks later than above symptoms
In large defects. The symptoms are more severe but they occur a few weeks later on than the children with moderate defects. The reason behind this is in larger defects, the pulmonary vascular medial remodeling starts and happens later and slower than those with smaller defects.
Chronic cough, hemoptysis, fatigue and exertional dyspnoea which appears later on. Development of pulmonary hypertension in long standing defect. Because of the high pulmonary blood flow, there is a resultant intimal proliferation of pulmonary resistance vessels. Chronic cough, hemoptysis, fatigue and exertional dyspnoea which appears later on.
Development of pulmonary hypertension in long standing defect. Because of the high pulmonary blood flow, there is a resultant intimal proliferation of pulmonary resistance vessels.
Hoarseness of cry Known as Ortners syndrome or cardiovocal hoarseness. With later stages of severe pulmonary hypertension. This is due to the compression of recurrent laryngeal nerve by the distended pulmonary artery. Hoarseness of cry
Known as Ortners syndrome or cardiovocal hoarseness. With later stages of severe pulmonary hypertension. This is due to the compression of recurrent laryngeal nerve by the distended pulmonary artery.
Parents noticing a bluish discoloration of the child's skin especially when crying. Onset of Eisenmengers syndrome, a more severe form of pulmonary hypertension. Parents noticing a bluish discoloration of the child's skin especially when crying.
Onset of Eisenmengers syndrome, a more severe form of pulmonary hypertension.

Clinicals - Examination

Fact Explanation
Refer to the growth chart: poor weight gain Especially in moderate to large defects, because the calorie requirement is higher, feeding difficulties and frequent respiratory tract infections. Usually a sensitive indicator of congestive cardiac failure. Refer to the growth chart: poor weight gain
Especially in moderate to large defects, because the calorie requirement is higher, feeding difficulties and frequent respiratory tract infections. Usually a sensitive indicator of congestive cardiac failure.
Profuse perspiration, evident as scalp sweating. After the onset of heart failure, sympathetic over-stimulation following increased cardiac demand. Profuse perspiration, evident as scalp sweating.
After the onset of heart failure, sympathetic over-stimulation following increased cardiac demand.
Duskiness of the skin, specially when the child is crying. Before the onset of pulmonary vascular hypertension, cyanosis is usually abset but when the cardiac requirement is high, there can be a mild duskiness of the skin colour depending on the size of the defect, more obvious in larger ones. Duskiness of the skin, specially when the child is crying.
Before the onset of pulmonary vascular hypertension, cyanosis is usually abset but when the cardiac requirement is high, there can be a mild duskiness of the skin colour depending on the size of the defect, more obvious in larger ones.
Mild tachypnoea In moderate to large defects. Due to heart failure and pulmonary congestion. Mild tachypnoea
In moderate to large defects. Due to heart failure and pulmonary congestion.
Tachycardia In moderate to large defects. Due to heart failure and sympathetic over-stimulation. Tachycardia
In moderate to large defects. Due to heart failure and sympathetic over-stimulation.
Systolic fluid thrill but apex is not displaced. In small defects. The turbulance that is caused by shooting of blood through the septal defect can be felt as a thrill at the apex. But the shunt is restrictive so the cardiac remodeling is usually minimal. Systolic fluid thrill but apex is not displaced.
In small defects. The turbulance that is caused by shooting of blood through the septal defect can be felt as a thrill at the apex. But the shunt is restrictive so the cardiac remodeling is usually minimal.
Hyperdynamic precordium: parasternal lift and apical thrust with a systolic thrill. In large defects. The volume overload causes ventricular dilatation and remodeling. The cardiomegaly is also a feature of heart failure. Hyperdynamic precordium: parasternal lift and apical thrust with a systolic thrill.
In large defects. The volume overload causes ventricular dilatation and remodeling. The cardiomegaly is also a feature of heart failure.
A localized harsh, holosystolic murmur which is best heard at the lower left sternal border, detected after 4-8 weeks of age or later. The murmur might end before the 2nd sound. In small defects which are <0.5 cm2. Usually other vital signs are normal. Throughout the systole, when the pressures of the both ventricles rise with myocardial contraction, the blood gushes from the left ventricle to the right through the narrow defect, giving rise to a localized, squeaky systolic murmur. The murmur becomes apparent only after the fall of pulmonary vascular resistance, which takes a few weeks after birth. A localized harsh, holosystolic murmur which is best heard at the lower left sternal border, detected after 4-8 weeks of age or later. The murmur might end before the 2nd sound.
In small defects which are <0.5 cm2. Usually other vital signs are normal. Throughout the systole, when the pressures of the both ventricles rise with myocardial contraction, the blood gushes from the left ventricle to the right through the narrow defect, giving rise to a localized, squeaky systolic murmur. The murmur becomes apparent only after the fall of pulmonary vascular resistance, which takes a few weeks after birth.
A low pitch holosystolic murmur which is best heard at the lower left sternal border. In larger defects, there the pressure difference between the right and left ventricles is small and thus the smaller turbulence. A low pitch holosystolic murmur which is best heard at the lower left sternal border.
In larger defects, there the pressure difference between the right and left ventricles is small and thus the smaller turbulence.
A mid diastolic rumble at the mitral area. Due to the functional mitral stenosis. A mid diastolic rumble at the mitral area.
Due to the functional mitral stenosis.
A loud pulmonic component of the second heart sound, and a systolic ejection murmur may be heard over the left sternal border. Fixed or paradoxical splitting of the second heart sound may be there. Due to secondary pulmonary hypertension. A loud pulmonic component of the second heart sound, and a systolic ejection murmur may be heard over the left sternal border. Fixed or paradoxical splitting of the second heart sound may be there.
Due to secondary pulmonary hypertension.
Cyanosis, bleeding manifestations and symptoms of deep vein thrombosis, heart failure along with pulmonary hypertension. Development of Eisenmengers syndrome. Cyanosis, bleeding manifestations and symptoms of deep vein thrombosis, heart failure along with pulmonary hypertension.
Development of Eisenmengers syndrome.
Disappearing murmur. In small VSDs, majority of the defects close between the age of 1-5 years. Disappearing murmur.
In small VSDs, majority of the defects close between the age of 1-5 years.

Investigations - Diagnosis

Fact Explanation
Chest radiography: erect, in full inspiration, postero-anterior and views. In small defects, the chest Xray film will reveal a normal sized heart and normal pulmonary vascular markings. In larger defects, it will show cardiomegaly. prominent main pulmonary artery segment with increased pulmonary vascular markings and enlarged left atrium. Once pulmonary hypertension develops, there will be right ventricular hypertrophy and reduced pulmonary vascularity in the outer third of the lung fields. Chest radiography: erect, in full inspiration, postero-anterior and views.
In small defects, the chest Xray film will reveal a normal sized heart and normal pulmonary vascular markings. In larger defects, it will show cardiomegaly. prominent main pulmonary artery segment with increased pulmonary vascular markings and enlarged left atrium. Once pulmonary hypertension develops, there will be right ventricular hypertrophy and reduced pulmonary vascularity in the outer third of the lung fields.
Echocardiograpghy Echocardiogram can be used to assess the defct and also the percutaneous treatment methods. . In context of the defect, Echocardiogram can be used to assess the number of drfects and their positions, and also the associated other cardiac defects. The rare swiss cheese septum, the multiple defects in the ventricular septum also can be identified. In addition, the complications, presence of heart failure and the ejection fraction also can be assessed. 3dimensional echo is better than 2 dimensional. Echocardiograpghy
Echocardiogram can be used to assess the defct and also the percutaneous treatment methods. . In context of the defect, Echocardiogram can be used to assess the number of drfects and their positions, and also the associated other cardiac defects. The rare swiss cheese septum, the multiple defects in the ventricular septum also can be identified. In addition, the complications, presence of heart failure and the ejection fraction also can be assessed. 3dimensional echo is better than 2 dimensional.
Magnetic Resonance Imaging MRI can be useful but used in infrequent requirements where most of the time reason is the Echocardiography is not adequate. But the systemic and pulmonary blood flow has been well described from MRI so, to assess the severity of left-to-right shunt, MRI is more useful. Magnetic Resonance Imaging
MRI can be useful but used in infrequent requirements where most of the time reason is the Echocardiography is not adequate. But the systemic and pulmonary blood flow has been well described from MRI so, to assess the severity of left-to-right shunt, MRI is more useful.
Doppler color flow ultrasonography and two-dimensional mapping. It is a valuable aid in the diagnosis of VSD and may be one reason for the observed increase in the incidence of VSD . It also allows the physician to assess overall prognosis by deciding the placement of the defect and presence of heart failure. It also can be used to follow up with time. Doppler color flow ultrasonography and two-dimensional mapping.
It is a valuable aid in the diagnosis of VSD and may be one reason for the observed increase in the incidence of VSD . It also allows the physician to assess overall prognosis by deciding the placement of the defect and presence of heart failure. It also can be used to follow up with time.
Electrocardiography The ECG changes depend on the cardiac manifestations by the defect, and that in turn essentially by the size of the defect. Small defects show no ECG changes. Moderate VSDs with significant left-to-right shunts with volume overload, left ventricular hypertrophy or even biventricular hypertrophy is the expected feature in ECG. The latter is known as Katz-Wachtel phenomenon. Left axis deviation is also a common finding.
In patients with large VSDs and equal ventricular pressures, right ventricular hypertrophy is expected. In patients with large pulmonary blood flow, left atrial hypertrophy is evidenced.
Electrocardiography
The ECG changes depend on the cardiac manifestations by the defect, and that in turn essentially by the size of the defect. Small defects show no ECG changes. Moderate VSDs with significant left-to-right shunts with volume overload, left ventricular hypertrophy or even biventricular hypertrophy is the expected feature in ECG. The latter is known as Katz-Wachtel phenomenon. Left axis deviation is also a common finding.
In patients with large VSDs and equal ventricular pressures, right ventricular hypertrophy is expected. In patients with large pulmonary blood flow, left atrial hypertrophy is evidenced.
Cardiac catheterization and angiography. In the previous studies it has been found that the sensitivity and specificity of this is not significant from that of Echocardiography. Cardiac catheterization and angiography.
In the previous studies it has been found that the sensitivity and specificity of this is not significant from that of Echocardiography.

Investigations - Management

Fact Explanation
Echocardiography To follow up the course of the defect and complications. It also can be used in follow up after corrective surgery. Echocardiography
To follow up the course of the defect and complications. It also can be used in follow up after corrective surgery.

Management - Supportive

Fact Explanation
Small VSD- No surgical management required. Observation with maintaining adequate oral hygiene is the management of choice. Studies have proved that a favorable evolution of the small VSD at long-term follow-up does not require surgical intervention, with concerns regarding the strict antibiotic prophylaxis. The overall clinical outcome of muscular VSD is better than that of the perimembranous type.
Surgical closure does not appear to be required during childhood as long as left-to-right shunt is <50% and signs of LV volume overload are absent, when pulmonary arterial pressure is not elevated, and no VSD-related Aortic Regurgitation or symptoms are present.
Small VSD- No surgical management required. Observation with maintaining adequate oral hygiene is the management of choice.
Studies have proved that a favorable evolution of the small VSD at long-term follow-up does not require surgical intervention, with concerns regarding the strict antibiotic prophylaxis. The overall clinical outcome of muscular VSD is better than that of the perimembranous type.
Surgical closure does not appear to be required during childhood as long as left-to-right shunt is <50% and signs of LV volume overload are absent, when pulmonary arterial pressure is not elevated, and no VSD-related Aortic Regurgitation or symptoms are present.
Antibiotic prophylaxis with oral penicillin. Prophylaxis is less necessary for patients who have documented complete closure of VSD. Fully repaired VSDs do not require long term antibiotic prophylaxis. The incidence of bacterial endocarditis with severity of the VSD is not clearly established, so unless the patients are going for dental or surgical procedures, it's not advisable to give long term antibiotic prophylaxis. Antibiotic prophylaxis with oral penicillin.
Prophylaxis is less necessary for patients who have documented complete closure of VSD. Fully repaired VSDs do not require long term antibiotic prophylaxis. The incidence of bacterial endocarditis with severity of the VSD is not clearly established, so unless the patients are going for dental or surgical procedures, it's not advisable to give long term antibiotic prophylaxis.
High calorie diet plan. Especially for the patients with heart failure or recurrent infections, and resultant growth faltering. Diet supplemented with high calorie food items will ensure adequate growth. High calorie diet plan.
Especially for the patients with heart failure or recurrent infections, and resultant growth faltering. Diet supplemented with high calorie food items will ensure adequate growth.

Management - Specific

Fact Explanation
Diuretics e.g. furosemide to relieve pulmonary congestion, reduce afterload and preload in cardiac failure. It is used as mainstay of treatment. Diuretics e.g. furosemide
to relieve pulmonary congestion, reduce afterload and preload in cardiac failure. It is used as mainstay of treatment.
Angiotensin-converting enzyme (ACE) inhibitors e.g. captopril and enalapril ACE inhibitors reduce both the systemic and pulmonary pressures, thereby reducing the left-to-right shunt. Angiotensin-converting enzyme (ACE) inhibitors e.g. captopril and enalapril
ACE inhibitors reduce both the systemic and pulmonary pressures, thereby reducing the left-to-right shunt.
Cardiac glycosides-Digoxin This may be indicated if symptoms do not respond to diuresis or ACE inhibition. Cardiac glycosides-Digoxin
This may be indicated if symptoms do not respond to diuresis or ACE inhibition.
Direct surgical repair Using cardiopulmonary bypass is the preferred surgical therapy. The long term outcome is better if the surgical correction is performed early. Caution in infants below 6months of age. Direct surgical repair
Using cardiopulmonary bypass is the preferred surgical therapy. The long term outcome is better if the surgical correction is performed early. Caution in infants below 6months of age.
Transatrial surgical approach. In perimembranous and inlet VSDs Transatrial surgical approach.
In perimembranous and inlet VSDs
Transcatheter therapy An experimental method where the VSD of perimembranous is repaired surgically and the VSDs in muscular septum are closed with a transcatheter device. This may be used for multiple VSDs Transcatheter therapy
An experimental method where the VSD of perimembranous is repaired surgically and the VSDs in muscular septum are closed with a transcatheter device. This may be used for multiple VSDs
Surgical correction of regurgitant aortic valves if present. Patients with perimembranous or muscular VSDs propose a higher risk for aortic valve prolapse and regurgitation, and also once a milder form of regurgitation has started it progresses rapidly to a severe form. Patients with perimembranous VSDs with AVP should be followed with serial echocardiography. Surgical correction of regurgitant aortic valves if present.
Patients with perimembranous or muscular VSDs propose a higher risk for aortic valve prolapse and regurgitation, and also once a milder form of regurgitation has started it progresses rapidly to a severe form. Patients with perimembranous VSDs with AVP should be followed with serial echocardiography.

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