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- 1. Atrial Septal Defects Dr.VANNALA RAJU Consultant Pediatrician Hyderabad
- 2. • Introduction • Anatrial septal defect (ASD) is a hole of variable size in the atrial septum. • ASD is detected in 1 child per 1500 live births, and accounts for 5-10% of congenital heart defects. • ASDs make up 30-40% of all congenital heart disease detected in adults (second only to bicuspid aortic valve). • ASDs occur in women 2-3 times more common than men.
- 3. • ASDs canoccur in different anatomic portions of the atrial septum. • ASDs can be isolated or occur with other congenital cardiac anomalies. • Functional consequences of ASDs are related to the anatomic location of the defect, its size, and the presence or absence of other cardiac anomalies.
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- 5. • Types ofASD • Primum ASD • Secundum ASD • Sinus venosus defects • Coronary sinus defects • Patent foramen ovale
- 6. • Primum ASD •• Make up ~15% of all ASDs. • • Occur if the septum primum does not fuse with the endocardial cushions, leavinga defect at the base of the interatrial septum that is usually large. • • Usually not isolated – primum ASDs are typically associated with anomalies of the AV valves (such as cleft mitral valve) and defects of the ventricular septum • (VSDs) or a common AV canal.
- 7. Secundum ASD • Makeup ~70% of all ASDs. • Occur twice as often in females. • Typically located within the area bordered by the limbus of the fossa ovalis. • Defects vary in size, from <3 mm to >20 mm.
- 8. • Secundum ASD •• May be associated with other ASDs. • • Multiple defects can be seen if the floor of the fossa ovalis (AKA valve of the foramen ovale) is fenestrated. • • Ten to twenty percent have a functional mitral valve prolapse. • • May be related to changing LV geometry associated with RV volume overload
- 9. Sinus venosus ASD •Make up ~10% of ASDs. • Characterized by malposition of the insertion of the SVC or IVC straddling the atrial septum. • Often associated with anomalous pulmonary venous return the RUL/RMLpulmonary veins may connect with the junction of the SVC and RA in the setting of a superior sinus venosus ASD.
- 10. • Coronary SinusSeptal Defects • • Less than 1% of ASDs • • Defects in the inferior/anterior atrial septum region that • includes the coronary sinus orifice. • • Defect of at least a portion of the common wall separating the coronary sinus and the left atrium – AKA “unroofed coronary sinus” • • Can be associated with a persistent left SVC draining into the coronary sinus.
- 11. • ASSOCIATIONS • Associatedmalformations are nearly 30%of Cases. Like: • Secundum ASD • ● Pulmonic stenosis • ● Mitral valve prolapse • ● Partial anomalous pulmonary venous connection • Primum ASD • ● Cleft mitral valve • ● Discrete subaortic stenosis • Sinus Venosus septal defect • ● Partial anomalous pulmonary venous return • Coronary Sinus septal defect • ● Partial and total anomalous pulmonary venous return • ● Persistent left superior vena cava
- 12. • Patent ForamenOvale • •Not truly an “ASD” because no • septal tissue is missing. • •Oxygenated blood from the IVC • crosses the foramen ovale in utero. • •At birth, the flap normally closes • due to Reduced right heart pressure and PVR • • Elevated LA pressure. • • Flap fusion is complete by age two • in 70-75% of children; the • remainder have a PFO.
- 13. LEFT-TO-RIGHT SHUNT • Inearly infancy, when pulmonary resistance is high, left and right ventricular compliances are similar, and net shunting through an ASD is typically slight. • As the left ventricle matures, it becomes less compliant in diastole than the right, and left atrial pressure rises. This drives a left-to-right shunt at the atrial level in the presence of an ASD. • With age, the disparity between systemic and pulmonary resistance, and in turn between left and right ventricular compliance, results in increased left-to- right shunting and advancing right ventricular volume loading. HEMODYNAMICS
- 14. Desaturated blood enters theright atrium from the vena cava at a volume of 3L/min/m2 and mixes with an additional 3 L of fully saturated blood shunting left to right across the ASD HEMODYNAMICS
- 15. Results in : increasein oxygen saturation in the right atrium. Six liters of blood flows through the tricuspid valve and causes a mid-diastolic flow rumble. Oxygen saturation may be slightly higher in the right ventricle because of incomplete mixing at the atrial level.
- 16. The full 6L flows across the right ventricular outflow tract and causes a systolic ejection flow murmur. Six liters returns to the left atrium, with 3 L shunting left to right across the defect and 3 L crossing the mitral valve to be ejected by the left ventricle into the ascending aorta.
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- 18. • Over time,right ventricular volume load results in dilation and hypertrophy, eventually affecting the function of both ventricles. • Atrial enlargement may contribute to the late incidence of atrial fibrillation. Right ventricular volume overload is noted to occur as a rule when ASDs are larger than 6 mm in diameter • Volume-induced hypertrophy of the right ventricle produces a loss of coronary reserve and eventual impairment of right ventricular systolic and diastolic function. • Left ventricular functional reserve is diminished by adulthood in most patients with ASD.
- 19. • • Althoughleft ventricular systolic function may be normal at rest, the left ventricle exhibits a subnormal diastolic dimension, and a loss of functional reserve at exercise. • • • In general, the functional loss in the left and right ventricles is normalized 6 months following ASD closure in children and young adults.
- 20. • NATURAL HISTORY •In patients with an ASD <3 mm in size • diagnosed before 3 months of age, • spontaneous closure occurs in 100% of • patients at 1½ years of age. • Spontaneous closure occurs more than 80% • in patients with defects between 3-8 mm • before 1½ years of age. • An ASD with a diameter > 8 mm rarely closes spontaneously.
- 21. • Natural Historyof ASDs • • Most ASDs <8mm close spontaneously in infants. • • Spontaneous closure is unusual in children and adults; defects often become progressively larger. • • Most patients with a significant shunt flow ratio (Qp:Qs > 2:1) will be symptomatic and require closure by age40. • • Increasing size of the ASD may preclude percutaneous closure. • • Weight is more affected then height • Association • • Holt oram syndrome • • Patau’s syndrome • • Edward’s syndrome
- 22. • • Ifuntreated, pulmonary hypertension and subsequent CCF may develop during or after third decade, and reversal of shunt may occur (rare), it may be progressive with pregnancy. • • With or without surgery, atrial arrhythmias (flutter or fibrillation) may occur in adults. • • Cerebrovascular accident, resulting from paradoxical embolization through an ASD, is a rare complication. Infective endocarditis does not occur in patients with isolated ASDs. Mitral stenosis may occur as a result of rheumatic fever in a case of ASD (Lutembacher syndrome).
- 23. • SYMPTOMS ANDSIGNS • Vary with the size of defect. • Small defect: • Asymptomatic and is usually diagnosed during a routine health check up. • Large defect: • Symptomatic and patients usually present with • Failure to thrive. • Easy fatigability. • Increased perspiration • Recurrent Pulmonary infections. • Platypnea
- 24. On examination • Generalexamination • Appearance: Usually normal • Heart rate: Normal • Respiratory rate: Normal • Weight and height: may be less than 10th centile.
- 25. • Precordium • Inspection: •Slight prominence of precordium • Palpation: • Apex beat may be shifted to left • P2 may be palpable • Left parasternal heave may be • present
- 26. Auscultation: • S1 isnormal • S2 is widely splitted and Fixed • Ejection systolic murmur, • medium pitched, soft, grade • 1-3/6 & best heard at left 2nd • & 3rd ICS • A diastolic flow rumble • across the tricuspid valve • region.
- 27. INVESTIGATIONS Routine tests : (CBC,septic screening, s.electrolyte, s. creatinine, blood grouping, coagulation profile, etc) should be done before management. Diagnostic Investigations includes- -X-ray -Ecg -Echocardiography -Sometimes cardiac catheterization
- 28. Xray Findings Cardiomegaly RA enlargement RVenlargement Full pulmonary conus Increased pulmonary vascular markings Plethoric lung fields
- 29. • Enlarged ‘p’wave indicating Right atrial hypertrophy. • rsR’ seen and tall R wave Indicating RBBB and RVH. • Also note that the aVF is predominantly upwards as compared to Lead I indicating Right Axis Deviation.
- 30. Echocardiogram Primary diagnostic imaging modalityfor ASD. Provides: - exact localization of ASD - size of ASD - measurement of septal rims - Confirmation of the shunt - Abnormal motion of ventricular septum. - Associated lesions can be identified
- 31. Cardiac catheterization Patients withthe classic features of a hemodynamically significant ASD on physical examination and chest radiography, in whom echocardiographic identification of an isolated secundum ASD is made, need not undergo diagnostic catheterization before repair. Exception: an older patient, in whom pulmonary vascular resistance may be a concern.
- 32. COMPLICATIONS OF ASD •Right sided heart failure • Frequent pulmonary infections • Flow-related PAH • Pulmonary vascular obstructive disease • Paradoxical embolism • Tricuspid and mitral insufficiency • Atrial arrhythmias—atrial flutter, atrial fibrillation,and Sick Sinus Syndrome.
- 33. MANAGEMENT • Patients withsmall shunts and normal RV size are generally asymptomatic and require no therapy but need longtime follow up for spontaneous closure • Moderate to large shunt and/or symptomatic ASD should be managed with following strategies: • Medical therapy • Interventional therapy • Surgical therapy
- 34. Medical management • Aimto reduce volume overload and to strengthen functions of heart muscles. Symptomatic children : • Diuretics: These agents relieve ventricular overload, peripheral and pulmonary congestion • Digoxin: Helps to strengthen the heart muscle, enabling it to pump more efficiently
- 35. Afterload reducers: • -Enalapril • - Captopril • Exercise restriction is no necessary • Prophylaxis for infective endocarditis is not Indicated • Atrial arrythmias : Appropriate Antiarrhythmic drugs. • Atrial fibrillation : Antiarrhythmic drugs and anticoagulants.
- 36. • Irreversible PAH:dobutamine, calcium channel blockers (high dose), diuretics, prostacycline, sildenafil or oxygen therapy. • Treatment of Other complications, likepulmonary infections, thrombo- embolic events or heart failure should also be treated accordingly.
- 37. . Closure of ASD: • In patients with small secundum ASDs and minimal left-to-right shunts without right ventricular enlargement, closure is not required Indications of ASD closure- • All symptomatic patients • Asymptomatic patients with- Qp : Qs ratio of at least 2 : 1 • Right ventricular enlargement • Time of closure- usually after the 1st yr and before entry into school
- 38. Interventional therapy Indication: 1. Echocardiographicevidence of ostium secundum ASD 2. Clinical evidence of RV volume load ( i.e. 1.5:1 degree of left to right shunt or RV enlargement) 3. ASD diameter less than 36 mm 4. Presence of sufficient rim of tissue( at least 5 mm) 5. Patient with fenestrated Fontan lateral tunnel if temporary balloon occlusion is tolerated
- 39. Contraindication: • Sinus venosus,coronary sinus or primum ASD • Extensive congenital cardiac anomaly • Known sepsis within one month prior to implantation or any untreated systemic infection prior to device placement. • Bleeding disorder, untreated ulcer or any other contraindications to aspirin therapy. • Demonstrated intracardiac thrombi on echo. • Any patient whose size or condition would cause to be a poor candidate for cardiac catheterization.
- 40. Different ASD closuredevices: • Clamshell(TM) device • Buttoned device • Angel wings(TM) device • Atrial septal defect occluder system device
- 41. Advantages of device closure- •It is safe and cost-effective than surgery • Successful implantation rates more than 96%, • Fewer complications: Major<1%, • Shortened hospitalization • Avoidance of pain and residual thoracotomy scars • Reduced need for blood products. Disadvantages of device closure- • Higher rate of small residual leak
- 42. Complications of DeviceClosure: • Device misalignment/embolization • Device erosion of atrial wall or aorta • Device impingement on adjacent structures AV valve, • Coronary sinus, SVC, Pulmonary veins, Aorta • Infection including endocarditis • Thromboembolic Complication • Allergic reaction • Valvular regurgitation • Residual shunt
- 43. Surgical management • Surgicalclosure has been the “gold standard” formof treatment of ASD. • Surgeons need proper training and expertise in performing operations. • The surgical approach can be by right thoracotomy or sternotomy, and more limited incisions are feasible with either approach.
- 44. • Procedure- Simple sutureor patch closure • Timing- Surgery is usually delayed until the patient is 2 to 4years of age because the • possibility of spontaneousclosure exists. • In infancy- If CCF not respond to medical management
- 46. Indications: • ASD withRA and RV enlargement with / without symptoms. • ASD minimum diameter > 10 mm on echocardiography • A sinus venosus, coronary sinus or primum ASD. • Chronic atrial arrythmia with ASD (concomitant Maze procedure) Contraindications: • Patients with severe irreversible PAH & reverse shunt SPO2 < 90%
- 47. Advantages of Surgery- •Can be performed in any type of ASD • Associated anatomical abnormality can be corrected concurrently. • Excellent late outcome. Disadvantages of Surgery- • Costly • Needs expertise hands • Prolong Hospital stay • pain and residual thoracotomy scars
- 48. Complications: ● Pericardial effusion/ constriction ● Residual shunt ● RV systolic and diastolic dysfunction ● Pulmonary artery pressure ● Mitral regurgitation ● Pulmonary vein stenosis or caval vein stenosis (sinus venosus defects) ● Arrhythmia ● Tricuspid regurgitation
- 49. Follow – UpAfter Surgical Closure: • Early postoperative follow-up: • -Symptoms of undue fever, fatigue, vomiting, chest pain, or • abdominal pain • ( may represent post pericardiotomy syndrome with • tamponade and needs immediate evaluation with • echocardiography.) • Annual clinical F/U: (if following conditions persist or • develop) • - PAH. • - Atrial arrhythmias. • - RV or LV dysfunction. • - Coexisting valvular or other cardiac lesion
- 50. TAKE –HOME MESSAGES •Atrial septal defects are relatively common CHD • Early symptoms are usually rare except very large • deffect. • Any kind of closure is safe and effective and • associated with improved life expectancy • A comprehensive treatment plan should include • input from the primary care provider, the • Paediatric Cardiologist and the Paediatric • Cardiovascular surgeon.
- 51. PROGNOSIS: • Patients generallysurvive up to adulthood without • surgical or percutaneous intervention mainly with • small to moderate size ASD and many patients live to • advanced age. • The results after surgical or device closure in • children with moderate to large shunts are excellent. • Mortality is less than 2% after surgical closure of • uncomplicated ASD • Mortality and morbidity increase with pulmonary • vascular disease
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