Ventricular Septal Defect

Published on 07/06/2015 by admin

Filed under Neonatal - Perinatal Medicine

Last modified 07/06/2015

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5 Ventricular Septal Defect


A 33-year-old white woman, gravida 4, para 3, was referred at 16 weeks’ gestation by the obstetrician for increased nuchal translucency (3.5 mm) at 12 weeks’ gestation.

D. Fetal management and counseling

1. Amniocentesis.

a. Because of the possibility of aneuploidy, amniocentesis was offered but was declined.

b. Abnormal karyotype with a single VSD is common in a fetus with a trisomy and otherwise structurally normal heart.

2. Follow-up.

a. Serial antenatal fetal echocardiography studies are performed at 6- to 8-week intervals to assess the size of the defect and compare it with the aortic root size serially.

b. At each visit, a renewed search is made for possible developing associated cardiac lesions, such as coarctation of the aorta.

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.

d. The size of the ascending aorta and transverse aortic arch is monitored.

e. Size and function of both ventricles are monitored. The size of the ventricles should be compared.

f. The size of the aortic valve annulus is monitored; check for subaortic stenosis.

g. The size and direction of flow across the foramen ovale should be checked to ensure the right-to-left flow is normal in the fetus.

h. The patency of the ductus arteriosus must be ensured.

i. Development of heart failure would not be expected in this condition.

j. Patient management options must be re-evaluated in view of any evolving lesions or new documentation of extracardiac findings that might alter the outcome.

F. Neonatal management

1. Medical.

With normal appearance and no other malformations, the baby should go home with the mother.

a. Heart failure with a VSD often does not manifest for several weeks after birth.

b. If the size of the arch is questionable, the baby should be managed as a neonate with possible coarctation (see Chapter 14).

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 imagep/images (ratio of pulmonary flow to systemic flow).

d. If the VSD is large and there is evidence of significant shunting, a high-calorie formula may be needed to maintain growth, given the high metabolic rate such infants can have.

2. Surgical.

a. The majority of VSDs (>50%) close spontaneously, usually in the first year of life. Only a small percentage of VSDs require surgery.

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

d. The risks of surgery are low: 1% to 2% for mortality or a complication such as complete heart block.

e. Contraindications for surgery after 1 year of age.