5 Ventricular Septal Defect
c. In an outlet defect, pulmonary stenosis can appear later in pregnancy, as evidenced by a pulmonary artery smaller than the aorta, thus evolving into tetralogy of Fallot or pulmonary valve stenosis.
2. Once the baby is delivered, an echocardiogram should be performed to determine the size, number, and hemodynamics of the VSD(s) and to exclude additional pathology. This could be done within the first 2 weeks of delivery if the third-trimester fetal echocardiogram suggests no critical heart disease.
c. Antifailure medication in the form of oral digoxin and furosemide can be started in the hospital, if surgery is likely, or at the first sign of congestive heart failure (see Chapter 30). Use of angiotensin-converting enzyme (ACE) inhibition to reduce the systemic vascular resistance out of proportion to the pulmonary vascular resistance can also assist in managing the heart failure by reducing the net shunting or p/s (ratio of pulmonary flow to systemic flow).
b. Surgery is confined to patients with elevation of pulmonary artery pressure, significant heart failure, failure to thrive, and evolution of additional pathology such as subaortic obstruction, aortic valve prolapse with regurgitation, and right ventricular outflow tract (RVOT) obstruction.
c. The surgical procedure of choice is primary open heart patch closure of the VSD and atrial septal defect (ASD) through the right atrium (RA) on bypass. Most patients are hospitalized 3 to 10 days after surgery for VSD and ASD closure
1. Subacute bacterial endocarditis (SBE) prophylaxis should be continued as long as any VSD is present and for 6 months after successful closure of the defect. ASD is not an indication for SBE prophylaxis.
2. Yearly visits to the cardiologist are indicated to detect late problems with arrhythmia such as sinus bradycardia from sinus node dysfunction or atrial tachycardia. A new heart murmur could indicate development of subaortic stenosis.
2. Echocardiogram confirmed the diagnosis of a large perimembranous VSD (Fig. 5-2), a small apical muscular VSD (Fig. 5-3), and a moderate-sized secundum ASD.
5. Surgery was performed at 2 months of age with division of the patent ductus arteriosus, patch closure of the secundum ASD, and patch closure of the VSD. Postoperatively, a large pericardial effusion developed that required pericardiocentesis.
7. At the 2-week follow-up visit in the cardiologist’s office, the baby was well and medications were stopped. SBE prophylaxis was continued for 6 months and then discontinued. He was seen yearly thereafter.
(Modified from Mullins CE, Mayer DC: Congenital Heart Disease: A Diagrammatic Atlas. New York, Liss, 1988.)
b. The spectrum of VSDs seen in prenatal life is very different from that manifesting postnatally. Isolated VSDs constituted only 6% of a large series of congenital heart diseases identified prenatally.
a. VSDs are the most common type of congenital heart malformation to be overlooked in the fetus. Their detection prenatally depends on the image quality, the size and site of the defect, and the color Doppler capabilities of the ultrasound machine. A large VSD may be seen only on imaging.