Guo Bule CPO Physiological Health Network 2001" May 31, 2001 18:47 Beijing Evening News
Beijing Evening News (Reporter Zhang Xuemei) reporter learned today from the Beijing Children's Hospital that: congenital heart disease has now become the first cause of death in children under the age of five. In our country, the incidence of congenital heart disease is seven to eight per thousand, that is to say, there are more than 100,000 small patients.
Beijing's child mortality monitoring shows: in recent years, children with congenital heart disease in infants and young children under the age of 5 years of the cause of death gradually moved forward, has risen from the third to the first. Experts believe that the cause of the rise of this disease is very complex, the cause is still unclear. However, it is now certain that there is a role for heredity and environmental pollution, as well as a cold virus or rubella virus infection in early pregnancy. Most congenital heart disease can be detected in the fetal period, i.e., in the mother's womb. In some developed countries, obstetrics departments have screening centers for CHD, and some pregnancies can be terminated after screening. Another thing is that early diagnosis and treatment can reduce infant and child mortality. In the past, due to the low level of treatment, some young children lost the best time for surgery. Li Zhongzhi, president of Beijing Children's Hospital, introduced: now the success rate of surgery for congenital heart disease has increased to 98%, and children should be operated promptly after birth. Children who have undergone surgery will not have disabilities, and some are now adults and athletes. Like the Beijing Children's Hospital, it is not uncommon for children born 10 days or so ago to have heart surgery, and last year they also operated on children born three days ago for congenital heart disease.
What should I look for in a child with congenital heart disease and fever?
Pediatric congenital heart disease is due to the developmental disorders of the heart during fetal life. The main causes are genetic and environmental factors.
Pediatric congenital heart disease is categorized in a variety of ways, the performance is not the same, but when infants, newborns appear the following symptoms, parents should be vigilant, timely medical treatment, in order to exclude cardiovascular malformation. The common manifestations include persistent cardiac and respiratory dysfunction after birth; persistent cyanosis or recurrent confusion; difficulty in breastfeeding and weight gain; detection of malformations other than cardiac; and recurrent "pneumonia"-like signs in the lungs.
Because children with congenital heart disease tend to be in poor health, poor nutrition, and have poor body defenses, they are susceptible to infections and fevers, and the disease evolves more rapidly and more severely. Repeated respiratory infections, in addition to fever, easy to complicate heart failure, etc., may therefore miss the opportunity to treat.
So when a child with congenital heart disease has a fever, it is important to seek medical attention and timely treatment. Usually, this kind of children should strengthen the care, patience feeding, warm and cold properly, try to prevent infection, in order to fight for the treatment time, improve the quality of survival of children.
Does tetralogy of Fallot affect a child's intellectual development?
Fallot's tetralogy of Fallot is the most common cyanotic congenital heart disease, accounting for about 70% of all patients with cyanotic congenital heart disease who survive beyond the age of 1 year.
Congenital heart disease is a heart malformation disease caused by abnormal development of the heart blood vessels during embryonic period, and it is the most common heart disease in children. Most mothers of affected children have viral infections during the third trimester of pregnancy, such as a history of rubella, mumps, and influenza, or have been exposed to radiation or certain toxic chemicals during pregnancy.
The manifestations of tetralogy of Fallot include cyanosis, which mostly occurs in the first 3 to 4 months of life, or cyanosis gradually becomes obvious after the closure of the arterial duct at about 1 year of age, and in severe cases, cyanosis occurs soon after birth. In severe cases, the bruising occurs soon after birth. The bruising is commonly seen on the lips, fingers, toes, tip of the nose, and ears. Because children with hypoxia are often short of breath, dyspnea becomes more pronounced and bruising worsens after crying, feeding, and activity. In most infants, paroxysmal dyspnea occurs suddenly during early morning feeding, and the bruising gradually worsens, which can lead to confusion, convulsions, and even death if it persists for a long period of time. Eighty percent of older children have squatting after activity, which relieves hypoxia and reduces the burden on the heart. Pediatrics are prone to pneumonia and heart failure. Due to long-term hypoxia, the growth of children is generally delayed, intellectual development is also slightly behind the normal children.
A doctor's examination may reveal a slight bulge on the left side of the chest, and a heart murmur may be heard; ultrasound of the heart and cardiac catheterization may help confirm the diagnosis.
The treatment of this disease is mainly surgical. Internal medicine treatment is mainly to deal with paroxysmal dyspnea, can be intravenous cardiac glycosides or subcutaneous morphine, can also be used sedatives, and timely correction of acidosis, oxygen. Long-term oral cardiac glycosides can reduce the episodes of paroxysmal dyspnea. Control heart failure with cardiotonic drugs. Antibiotics should be used before and after surgery to prevent endocarditis.
Fallot's tetralogy of Fallot is harmful to children, systemic hypoxia is obvious, especially brain hypoxia can affect the growth and intellectual development of children, so it should be prevented. Pregnant women in the first three months of pregnancy to avoid infection, avoid contact with patients, less to the public **** place, do not smoke, do not drink alcohol, avoid contact with radiation and some toxic chemicals.
Congenital heart disease
Congenital heart disease (congenital heart disease) is an abnormality in the development of the heart and large blood vessels during the embryonic period, also known as congenital cardiac malformation. Congenital heart disease is the most common heart disease in newborns and children (especially children under 4 years old). Its etiology and pathogenesis are not yet fully understood, and it is generally believed that it is mainly due to the presence of certain harmful factors (e.g. viral infections, etc.) in the mother's body during the early embryonic period (5-8 weeks of gestation, i.e., the most important period of embryonic cardiac development), which affects the normal development of the heart. Some congenital heart diseases may be related to genetic factors.
There are many types of congenital malformations of cardiovascular development because of the complexity of the heart development process and structure of the embryo. Common types are shown in Table 8-1:
Table 8-1 Common types of congenital cardiovascular developmental malformations
Types
Percentage of congenital heart disease
Non-cyanotic
Ventricular septal defect
25% to 30%
Arterial duct opening
17% to 20%
Atrial septal defect
10% to 15%
Cyanotic type
Tetralogy of Fallot
8% to 15%
Massive vascular displacement
8% to 10%
Other types
Aortic stenosis
5% to 7%
Pulmonary stenosis
5% to 7%
Aortic orifice stenosis 4% to 5%
Additionally, bicaval and tricaval hearts, perpetual trunks, double aortic arches, mitral and tricuspid insufficiency, and left coronary artery originating from the pulmonary artery are rare.
I. Two-chambered and three-chambered hearts
Two-chambered and three-chambered hearts are the result of an underdeveloped atrial and/or ventricular septum. A completely undeveloped atrial and ventricular septum results in a two-chambered heart with one room and one chamber. An undeveloped septum or one of the interventricular septa results in a three-chambered heart (one room, two chambers or two rooms, one chamber). Because of the complete mixing of arterial and venous blood in this type of cardiac malformation, the child is born with cyanosis and dies soon after birth.
Two, atrial septal defect
Embryonic development in the fifth week, from the original total atrium of the left and right part of the first septum between the two parts of the growth of the first septum (the first atrial septum), from the back of the upward and downward growth, so that the two atria between the two parts of the heart is still open (known as the first atrial foramen ovale) is gradually narrowed and continue to grow downward, and the endocardial pads and ventricular septum healing and complete closure. However, before the first interatrial foramen is completely closed, the upper part of the first interatrial septum splits to form the second interatrial foramen.
During the sixth week of embryonic development, a second septum (the second septum) grows to the right of the first septum and grows forward just enough to cover the second atrial foramen like a side curtain, but blood flow in the right-to-left direction can still pass through. The channel formed by the first and second septum is the foramen ovale. After birth, the lungs open and a large amount of blood enters the left atrium from the pulmonary veins, creating a pressure differential from the left to the right atrium that brings the upper part of the first septum closer to the second septum, with which it usually heals later. The foramen ovale remains anatomically open in about 25% of toddlers and children, but is closed because the left atrium has a higher pressure than the right atrium.
1. Second interatrial septal defect A gap or gaps in the fossa ovalis (also known as a fossa ovalis defect), the largest being the entire fossa ovalis. It occurs when the physiologic crack in the upper part of the first septum, which normally forms the second foramen ovale, occurs in the wrong position or is too large to be covered by the second septum, resulting in the survival of a defective second foramen ovale. Thus, it is not actually the second interatrial septum that is defective, but rather the second interatrial foramen in the first interatrial septum.
Postnatal shunting from the left atrium to the right atrium is caused by increased pulmonary blood flow, which increases left atrial pressure (Figure 8-45). The patient has no cyanosis. In larger defects, the right heart suffers right ventricular hypertrophy and pulmonary hypertension due to increased volume loading. Severe cases may cause secondary reverse shunting (right atrial to left atrial shunt) leading to cyanosis.
Figure 8-45 Pattern of atrial septal defect
1. superior vena cava 2. inferior vena cava 3. right atrium 4. right ventricle 5. pulmonary vein 6. left atrium 7. left ventricle 8. pulmonary artery 9. aorta
2. first interatrial septal defect An isolated first interatrial foramen and first interatrial septal defect is a partial absence of the interatrial septum at the level of the AV valve. Isolated first atrial septal defects are due to impaired growth of the first atrial septum and the endocardial cushion is not involved. However, most cases tend to be complicated by incomplete or non-healing of the endocardial cushion of the atrioventricular canal, and therefore it is extremely rare to have an intact mitral valve, tricuspid valve, and ventricular septum (there can be either partial or complete atrioventricular canal perpetuation).
Hemodynamic deficits in isolated first ventricular septal defects are similar to those in second ventricular foramen defects and have a better prognosis. If combined with endocardial cushion defects, there may be mitral and/or tricuspid valve closure insufficiency in addition to left-to-right shunting at the level of the atria, as well as left-to-right shunting at the level of the ventricles.
Three, ventricular septal defects
In the sixth week of embryonic development, a muscular septum (interventricular septum) grows from the bottom up between the left and right ventricles. At first, a connection between the two ventricles (interventricular foramen) remains between its upper edge and the two endocardial cushions. By week 8, it closes, and a membrane-like portion of the ventricular septum occurs. Growth defects and/or failure to fuse the various components that make up the ventricular septum can result in ventricular septal defects.
The most common ventricular septal defect is a high-grade membranous defect (Fig. 8-46), and in rare cases, a small foramen ovale-like defect occurs in the muscular portion of the ventricular septum.
Figure 8-46 Pattern of ventricular septal defects
1. left atrium 2. left ventricle 3. right atrium 4. right ventricle 5. superior vena cava 6. inferior vena cava 7. aorta 8. pulmonary artery 9. pulmonary vein
Individual ventricular septal defects of the membranous portion of the ventricular septum are usually small. During ventricular systole, the pressure in the left ventricle is higher than that in the right ventricle, and part of the blood is shunted into the right ventricle, thus increasing the volume of blood in the right ventricle and the volume of blood entering the pulmonary circulation. As a result, the blood volume of the right ventricle increases, and the volume of blood entering the pulmonary circulation increases. As a result, the volume of blood returning from the pulmonary veins to the left heart also increases, which can eventually lead to the dilatation and hypertrophy of the right ventricle, the pulmonary artery, the left ventricle, and the left atrium. When the defect is very small, the amount of blood shunted to the right ventricle is very small, but the blood flow through the narrow hole can be a large vortex, and a clear systolic murmur can be heard on clinical auscultation.
Four, Fallot tetralogy
Fallot tetralogy (tetralogy of Fallot) was first described by Fallot (1888). This cardiac malformation is characterized by four features: (1) narrowing of the pulmonary outflow tract; (2) a large defect in the membranous portion of the ventricular septum; (3) a rightward shift of the aorta, which rides above the ventricular septal defect; and (4) a highly hypertrophied and dilated right ventricle (Figure 8-47).
Figure 8-47 Fallot's tetralogy of Fallot pattern
Pulmonary artery stenosis with a giant defect in the membranous portion of the interventricular septum, the aorta shifted to the right and riding over the interventricular septum, and the right ventricle with high hypertrophy and dilatation of the cardiac chambers
This abnormality occurs due to the developmental dysplasia of the pulmonary artery muscular cones associated with the stenosis, the misaligned supraventricular crusade, and the failure of the cones to fuse with the muscular interventricular septum, which result resulting in a high-grade ventricular septal defect with membranous defects.
Pulmonary stenosis is most often seen in the pulmonary valve orifices and less commonly in the pulmonary trunk and conus arteriosus. Compensatory hypertrophy of the right ventricle occurs due to obstruction of blood input to the lungs.
With a large defect in the interventricular septum, during cardiac systole, part of the blood is shunted from the left ventricle into the right ventricle, so that the blood volume of the right ventricle is increased and compensatory dilatation and hypertrophy occur.
In addition, because the aorta rides on top of the septal defect and receives a large amount of blood from the left and right ventricles at the same time, resulting in lumen dilatation and wall thickening, the more the pulmonary artery is narrowed, the more the right ventricle injects into the aorta, and the more pronounced the dilatation and hypertrophy of the aorta. The enlarged aorta contrasts sharply with the narrowed pulmonary artery. In a small number of children, there may be other cardiac anomalies, such as an aorta located on the right side of the heart.
Clinically, the child has marked cyanosis, which is more pronounced the more severe the pulmonary artery stenosis. This is because the high degree of narrowing of the pulmonary artery, on the one hand, prompted the right ventricle of the venous blood more shunt into the aorta, on the other hand, the right ventricle of the blood is difficult to inject into the pulmonary circulation for gas exchange. x-ray, the right ventricle is highly hypertrophic, the lungs due to the reduction in the amount of blood inflow shows a reduction in the lung texture, lung field is abnormally transparent, clear.
Children usually survive for many years, and a few reach adulthood due to the compensatory effect of collateral circulation. The bronchial arteries often show compensatory dilatation, and the collateral circulation between the pulmonary and bronchial arteries allows blood from the aorta to enter the lungs via the collateral branches and be compensated. In rare cases, there is a combination of patent ductus arteriosus, and the dilated ductus arteriosus becomes an important collateral circulation. Surgical treatment is feasible for this disease.
V. Opening of the ductus arteriosus
The ductus arteriosus is a short arterial conduit that connects the pulmonary artery to the aorta during the fetal period. At birth, the ductus arteriosus has a diameter of about half of the diameter of the aorta, and gradually becomes atretic later. Physiologic atresia usually occurs at birth, or about six months after birth, and in a few cases can be delayed until a year later.
A patent ductus arteriosus is a completely unobstructed or only partially unobstructed duct (Figure 8-48). This malformation can occur alone or in combination with other cardiac malformations (atrial septal defect, ventricular septal defect, pulmonary stenosis, etc). When the ductus arteriosus is open alone, the amount of blood shunted from the aorta to the pulmonary artery is very high. Since the blood flows from the aorta (arterial blood) into the pulmonary artery, the child does not have cyanosis. Surgical ligation of a patent ductus arteriosus can be curative.
Figure 8-48 Pattern of arterial duct failure
1. superior vena cava, 2. inferior vena cava, 3. right atrium, 4. right ventricle, 5. pulmonary vein, 6. left atrium, 7. left ventricle, 8. pulmonary artery, 9. aorta, 10. arterial conduit
6. aortic coarctation
Aortic coarctation (coarctation of the aorta) is a non-cyanotic congenital condition. Coarctation of the aorta is one of the more common types of non-cyanotic congenital heart disease. The disease is divided into juvenile and adult types:
1. Juvenile type is a narrowing of the isthmus of the aorta before the ductus arteriosus. The stenosis is often severe, reducing the amount of blood passing through the aorta. This type is often combined with an open ductus arteriosus malformation, part of the venous blood in the pulmonary artery can be injected into the descending aorta through the open ductus arteriosus, therefore, the patient's lower extremity arterial blood is low in oxygen, and thus severe cyanosis, while the upper extremity arterial blood is normal in oxygen content. Infants born with atresia of the ductus arteriosus do not survive.
2. The adult form is a stenosis of the isthmus of the aorta behind the ductus arteriosus. The stenosis is usually mild and the ductus arteriosus is usually atretic. Because the stenosis is located distal to the ductus arteriosus, there is a high pressure difference between the thoracic aorta and the abdominal aorta. Compensatory adaptation occurs over time, as the arterial branches of the aortic arch (thoracic arteries, internal mammary artery and its intercostal branches) gradually dilate and collateral circulation occurs with the branches of the descending aorta (intercostal arteries, deep abdominal arteries, etc.) in order to ensure the blood supply to the lower limbs.
VII. Transposition of the great vessels
Transposition of the great vessels is an abnormality of the aorta and pulmonary artery in the process of embryonic transposition, which can be divided into corrective and non-corrective types.
1. Corrective type The aorta is displaced anteriorly and the pulmonary artery is displaced posteriorly, and the two are arranged in parallel anteroposteriorly and posteriorly. However, this is usually accompanied by reciprocal displacement of the right and left ventricles. Thus, the aorta is still from the left ventricle and the pulmonary artery is from the right ventricle. Circulation is normal and the patient is asymptomatic and healthy.
2. Uncorrected type The aorta and the pulmonary artery have switched places, i.e., the aorta is from the right ventricle and the pulmonary artery is from the left ventricle; the aorta is located on the right anterior side of the pulmonary artery, and there is no normal form of crossing of the aorta and pulmonary artery, which are in parallel arrangement. Blood from the right ventricle is not injected into the lungs for gas exchange, but is injected into the general circulation by the aorta; blood from the left ventricle is not injected into the whole body, but is injected into the lungs via the pulmonary artery. Non-corrected (also known as complete) transposition of the great vessels has no major effect on embryonic development during the embryonic period because of the presence of the umbilical vein, which is communicated by an arterial conduit. After birth, the lungs begin to breathe, the child becomes cyanotic, and if there is no other blood pathway to the heart, death occurs soon after birth. Those who survive after birth have a combination of other malformations that present abnormal pathways between the major and minor circulations, such as patent foramen ovale, patent ductus arteriosus, atrial septal defects, and ventricular septal defects. These anomalous pathways allow some of the blood to mix, supplying systemic needs and sustaining life.