The probability of spontaneous recovery of neonatal ventricular septal defect

I believe that many people are not very familiar with the condition of neonatal ventricular septal defect, because it is a professional medical term. It mainly refers to a condition caused by congenital heart problems. Many people do not know much about this disease, and are even less aware of its harm. Many people are concerned about whether this condition in newborns can heal itself. Now let us learn about the chances of curing neonatal ventricular septal defect through the following article.

Generally speaking, simple atrial septal defect and ventricular septal defect have the possibility of healing naturally under certain conditions, but in this case, atrial septal defect combined with ventricular septal defect is generally difficult to heal spontaneously. As two common congenital heart diseases, atrial septal defect and ventricular septal defect have independent

Characteristics. If it is a simple atrial or ventricular septal defect, if the defect is smaller than 0.3 cm, it can basically heal itself before the age of one. If it is smaller than 0.5 cm, there is a high possibility of self-healing. If it is smaller than 1 cm, there is also a certain possibility of self-healing before the child is one year old. However, if it is larger than 1cm and older than one year old, there is basically no possibility of natural healing. In the case of atrial septal defect combined with ventricular septal defect, it is basically difficult to heal on its own. Even if the conditions are possible for self-healing, since it is a combined congenital heart disease, it is impossible to heal on its own.

Ventricular septal defect (VSD) is one of the most common types of congenital heart disease in children. It can exist alone or in combination with other cardiovascular malformations. About half of the survivors of cyanotic congenital heart disease have ventricular septal defect.

Causes

The defect can occur in any part of the ventricular septum. According to the location of the defect, it can be divided into: ① Perimembranous ventricular septal defect: the most common, accounting for 60% to 70%, located in the membranous part of the ventricular septum and involving the adjacent muscular ventricular septum. According to the extension direction of the defect, it can be divided into perimembranous inflow tract type, perimembranous trabecular type and perimembranous outflow tract type. Large defects may extend to two or more parts, which is called perimembranous fusion type. ② Muscular ventricular septal defect: accounts for 15% to 25%, with the membranous part intact. According to the location, it can be divided into muscular inflow tract type, muscular trabecular type and muscular outflow tract type. The latter is separated from the pulmonary valve by muscle. ③ Biarterial subvalvular type: also known as subpulmonary valve type, accounting for 3% to 6%, but the incidence can reach 29% in the Oriental population. Its main feature is that the upper edge of the defect is the connection between the aorta and the pulmonary valve ring, the cone ventricular septum is poorly developed or absent, and the left-to-right shunt can be reduced when the coronary valve prolapses, but it is easy to cause aortic valve regurgitation. In some perimembranous defects, especially perimembranous inflow ventricular septal defects, fibrous tissue derived from the tricuspid valve can be seen adhering to the edge of the defect, forming a pseudoventricular septal aneurysm, which reduces the defect or completely blocks shunt and achieves natural closure. Most defects are single, but multiple defects may also occur. It may be combined with atrial septal defect, patent ductus arteriosus or aortic coarctation.

Clinical manifestations

Depends on the size of the defect, pulmonary blood flow and pressure. Small defects, small shunt flow, usually have no clinical symptoms. Moderate defects may cause symptoms in infancy. Large defects will cause shortness of breath and sweating 1 to 2 months after birth, frequent interruptions when sucking milk due to shortness of breath, slow weight gain, and pale complexion. When accompanied by chronic left ventricular failure, the patient often feels restless at night and has an "asthma"-like wheezing sound. Young children often have respiratory infections and are susceptible to pneumonia. Older children may experience symptoms such as weight loss, shortness of breath, palpitations, and fatigue. Sometimes hoarseness is caused by compression of the recurrent laryngeal nerve by the dilated pulmonary artery. In the late stage (more common in children or adolescents) or in patients with a large defect and obvious pulmonary artery hypertension, right-to-left shunting may occur, cyanosis may occur, and the condition may gradually worsen. If the defect shrinks with age, symptoms will also be alleviated.

treat

1. Medical treatment mainly prevents and treats infective endocarditis, lung infection and heart failure. By administering digitalis, diuretics, limiting salt intake and/or reducing afterload, and actively treating respiratory tract infections, heart failure in children can be controlled and their normal growth and development can be ensured. Percutaneous interventional occlusion: Percutaneous interventional occlusion is often the first choice for simple VSD after 2 years of age.

2. Surgical treatment: Patients with large defects who develop congestive heart failure that is difficult to control medically within 6 months, including repeated pneumonia and slow growth, should be treated surgically. Children aged 6 months to 2 years, although heart failure can be controlled, should also undergo surgical repair in a timely manner if pulmonary artery pressure continues to increase and is greater than 1/2 of the systemic arterial pressure, or if the ratio of pulmonary circulation to systemic circulation is greater than 2:1 after 2 years of age. Surgery is not suitable for patients with advanced organic pulmonary hypertension with bidirectional or right-to-left shunt.