Interatrial Septal Defect – Diagnosis And Treatment
Interatrial septal defect is an anatomical defect of the interatrial septum that allows a communication between the left atrium and the right atrium. During intrauterine life, foramen ovale assures the blood flow from the right atrium into the left atrium, because the lungs are deprived of blood circulation. Lack of closure of foramen ovale, causes the defect known as interatrial septal defect type fossa ovale. Interatrial septal defect incidence is 10% of congenital heart malformative diseases. It is a congenital heart malformation with left-right shunt and increased pulmonary flow.
Depending on the location of parietal defect, the interatrial septal defect has following types:
- Foramen ovale interatrial septal defect – persistent foramen ovale give a small defect, which is different from the ostium secundum interatrial septal defect only by smaller sizes, because is located in the same area were is located ostium secundum interatrial septal defect.
- Ostium secundum interatrial septal defect – a greater lack of interatrial septum characterizes this type of defect located in the middle portion of the interatrial wall. Is the most common type, because it represents 70% of all interatrial septal defects. Sometimes it can appear as a membrane with many perforations. Association of Ostium secundum interatrial septal defect and mitral stenosis is known as Lutembacher syndrome.
- Interatrial ostium primum septal defect – defect is located in the lower part of interatrial septum associated with atrioventricular valvular defect.
- Coronary sinus interatrial septal defect – the absence of interatrial wall at the site of drainage of coronary venous sinus.
- Venous sinus interatrial septal defect – represents a superior location of the defect at the shedding of the superior vena cava. In some cases is associated with partial pulmonary venous drainage.
- Unique atrium interatrial septal defect – when the interatrial septum is totally absent but the valvular structures (mitral and tricuspid) are normal.
The parietal defect produces a left-right shunt. Due to higher pressure, blood passes from the left atrium into the right atrium, pulmonary circulation load, leading in time to the installation of a pulmonary vascular hypertension. Volume of blood is dependent on the size of the defect, right ventricular compliance and pulmonary vascular resistance. Pulmonary stasis predisposes to recurrent infections. Long evolution of a large interatrial septal defect, can lead to irreversible pulmonary vascular hypertension, with installation of Eisemenger syndrome, characterized by cyanosis and cardiac decompensation, because the shunt is reversed from left-right shunt to a right-left shunt.
The majority of interatrial septal defects, even those defects wich are signifiant remain asymptomatic hemodynamically and are discovered incidentally during medical examinations or when they become symptomatic in the second or third decade of life. At clinical examination can be detected an ejection systolic murmur in pulmonary focus given by increasing of the blood flow through the pulmonary valve and duplication of the second cardiac sound. The symptoms that appear in children and young adults are: asthenia, fatigue and shortness of breath with exercise, palpitations given by atrial extrasystoles or by the installation of atrial fibrillation.
Diagnosis of interatrial septal defect:
The clinical suspicion of interatrial septal defect is confirmed by laboratory investigations:
- Cardiothoracic radiography: heart shadow is increased by the enlarged right atrium and right ventricle associated with pulmonary stasis.
- Echocardiography: is the most simple and reliable method that specify the diagnosis, location, size, direction of the shunt, hemodynamic implications of the right ventricle, tricuspid valve and estimates the left ventricular function. This exploration can exclude other associated anomalies such as mitral regurgitation, Ebstein disease or ventricular septal defect.
- Cardiac catheterization, interatrial septal defect can be confirmed by passing of the probe from the right atrium into the left atrium. The interatrial septal defect with a long evolution, with severe pulmonary hypertension represents a indication for cardiac catheterization to assess the reversibility of pulmonary hypertension or if is contraindicated for surgery. Is a procedure that is indicated of routine in patients with interatrial septal defect, over 45 years to exclude a coronary artery disease.
The treatment of interatrial septal defect is exclusively surgical. Interatrial septal defect closure is recommended for all uncomplicated cases with significant shunt left-right and pulmonary blood flow / systemic blood flow ration greater than 1.5. Ideally this should be done at the age of 2-4 years. To children with small and trivial defect is not indicated surgery and they are checked periodically.
Interatrial septal defect closure may be made:
- Interventional – by placing a device in the catheterization laboratory, which will close the defect, avoiding surgery.
- Surgical, which can be done:
- Conventional, when the parietal defect is closed by direct suturing if is small or using a pericardium patch or a textile patch, which closes the defect, if the interatrial septal defect is important.
- Robotic surgical method, the difference from the classical approach is made by the small incisions, by a better esthetic result and by a reduced hospitalization period by reducing the surgical trauma.
Postoperative evolution is easy in most cases. Postoperative mortality must be zero or less than 1%, even in cases with long evolution and preoperative complications (embolism, arrhythmias, endocarditis). Locked in time, quality of life is identical to that of the general population.