Open ductus arteriosus - description, symptoms (signs), treatment. Patent ductus arteriosus Vps patent ductus arteriosus ICD 10
Patent ductus arteriosus is a non-closure of the accessory vessel connecting the aorta and pulmonary artery, which continues to function after the period of its obliteration has expired. The ductus arteriosus (dustus arteriosus) is an essential anatomical structure in the embryonic circulatory system. However, after birth, due to the appearance of pulmonary respiration, the need for the ductus arteriosus disappears, it ceases to function and gradually closes. Normally, the functioning of the duct ceases in the first 15-20 hours after birth, complete anatomical closure lasts from 2 to 8 weeks.
In cardiology, patent ductus arteriosus accounts for 9.8% of all congenital heart defects and is diagnosed 2 times more often in women. Patent ductus arteriosus occurs both in isolated form and in combination with other anomalies of the heart and blood vessels (5-10%): stenosis of the aortic mouth, stenosis and atresia of the pulmonary arteries, coarctation of the aorta, patent atrioventricular canal, VSD, ASD, etc. For defects hearts with ductus-dependent circulation (transposition of the great arteries, extreme form of tetralogy of Fallot, interruption of the aortic arch, critical pulmonary or aortic stenosis, left ventricular hypoplasia syndrome), the patent ductus arteriosus is a vital concomitant communication.
Features of hemodynamics with patent ductus arteriosus.
The patent ductus arteriosus is located in the upper floor of the anterior mediastinum; it originates from the aortic arch at the level of the left subclavian artery and flows into the pulmonary trunk at its bifurcation and partially into the left pulmonary artery; sometimes there is a right-sided or bilateral ductus arteriosus. The ductus botallus can have a cylindrical, cone-shaped, fenestrated, aneurysmal shape; its length is 3-25 mm, width – 3-15.The ductus arteriosus and the patent foramen ovale are necessary physiological components of the fetal circulation. In the fetus, blood from the right ventricle enters the pulmonary artery, and from there (since the lungs do not function) through the ductus arteriosus into the descending aorta. Immediately after birth, with the newborn's first spontaneous breath, pulmonary resistance falls and pressure in the aorta rises, leading to the development of shunting of blood from the aorta into the pulmonary artery. The inclusion of pulmonary respiration promotes spasm of the duct due to contraction of its smooth muscle wall. Functional closure of the ductus arteriosus in full-term infants occurs within 15-20 hours after birth. However, complete anatomical obliteration of the Botallian duct occurs by 2-8 weeks of extrauterine life.
A patent ductus arteriosus is said to exist if its functioning does not stop 2 weeks after birth. Patent ductus arteriosus is a pale type defect because it causes oxygenated blood to be discharged from the aorta into the pulmonary artery. Arteriovenous shunting causes additional volumes of blood to enter the lungs, congestion of the pulmonary vascular bed and the development of pulmonary hypertension. The increased volume load on the left parts of the heart leads to their hypertrophy and dilatation.
Hemodynamic disturbances with a patent ductus arteriosus depend on the size of the message, the angle of its origin from the aorta, and the pressure difference between the systemic and pulmonary circulation. Thus, a long, thin, tortuous duct, extending at an acute angle from the aorta, resists the reverse flow of blood and prevents the development of significant hemodynamic disorders. Over time, such a duct can become obliterated on its own. The presence of a short, wide open ductus arteriosus, on the contrary, causes significant arteriovenous discharge and pronounced hemodynamic disorders. Such ducts are not capable of obliteration.
Small anomalies of heart development: Brief description
Small anomalies heart development(MARS) - anatomical congenital changes in the heart and great vessels that do not lead to gross dysfunction of the cardiovascular system. A number of MARS are unstable and disappear with age.
Etiology
Hereditary determined connective tissue dysplasia. A number of MARS are dysembryogenetic in nature. The influence of various environmental factors (chemical, physical effects) cannot be excluded.
Code according to the international classification of diseases ICD-10:
Q24.9 Congenital heart defect, unspecified
Other diagnoses in the ICD 10 section
Q24.0 Dextrocardia Q24.1 Levocardia Q24.2 Triatrial heart Q24.3 Infundibular stenosis of the pulmonary valve Q24.4 Congenital subaortic stenosis
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Heart defects.congenital (classification)
Classification of congenital heart disease by severity classes (J. Kirklin et al. 1981) class I. It is possible to perform a planned operation later than 6 months: VSD, ASD, radical correction for tetralogy of Fallot class II. A planned operation can be performed within 3–6 months: radical correction for VSD, open atrioventricular canal (PAVC), palliative correction for class III TF. A planned operation can be performed within a period of up to several weeks: radical correction for transposition of the great vessels (TMS) class IV. Emergency surgery with a maximum preparation period of several days: radical correction for total anomalous pulmonary vein drainage (TAPDV), palliative correction for TMS, VSD, OAVC class V. The operation is performed urgently due to cardiogenic shock: various types of defects in the decompensation stage.
Classification of congenital heart disease by prognostic groups(Fyler D. 1980) 1 group. Relatively favorable prognosis (mortality during the first year of life does not exceed 8–11%): patent ductus arteriosus, VSD, ASD, pulmonary stenosis, etc. Group 2. Relatively unfavorable prognosis (mortality during the first year of life is 24–36%): tetralogy of Fallot, myocardial diseases, etc. Group 3. Poor prognosis (mortality during the first year of life is 36–52%): TMS, coarctation and stenosis of the aorta, tricuspid valve atresia, TADLV, single ventricle of the heart, OAVC, origin of the aorta and pulmonary artery from the right ventricle, etc. Group 4. Extremely unfavorable prognosis (mortality during the first year of life is 73–97%): hypoplasia of the left ventricle, pulmonary atresia with an intact interventricular septum, common truncus arteriosus, etc.
Classification of congenital heart disease according to the possibility of radical correction(Turley K. et al. 1980) 1 group. Defects for which only radical correction is possible: aortic stenosis, pulmonary artery stenosis, TADLV, triatrial heart, coarctation of the aorta, patent ductus arteriosus, aortic pulmonary septal defect, ASD, mitral valve stenosis or insufficiency group 2. Defects in which the advisability of radical or palliative surgery depends on the anatomy of the defect, the age of the child and the experience of the cardiology center: various variants of TMS, pulmonary atresia, common truncus arteriosus, tetralogy of Fallot, OAVC, VSD group 3. Defects for which only palliative operations are possible in infancy: a single ventricle of the heart, some variants of the origin of the great vessels from the right or left ventricle with pulmonary stenosis, atresia of the tricuspid valve, atresia of the mitral valve, hypoplasia of the ventricles of the heart.
Abbreviations OAVC - open atrioventricular canal TMS - transposition of the great vessels TADLV - total anomalous drainage of the pulmonary veins.
ICD-10 Q20 Congenital anomalies of the heart chambers and connections Q21 Congenital anomalies of the cardiac septum Q22 Congenital anomalies of the pulmonary and tricuspid valves Q23 Congenital anomalies of the aortic and mitral valves Q24 Other congenital anomalies of the heart.
More than 400 children with developmental anomalies were born in Kyrgyzstan during the year.
Since there are a lot of defects of the circulatory system, there cannot be only one VSP code according to ICD 10. In addition, the clinical picture of some of them is so similar that modern informative diagnostic techniques have to be used for differentiation.
There is a huge difference between acquired cardiac disorders and congenital developmental anomalies, as they are in different ICD classes. Although the disturbances in arterial and venous blood flow will be the same, the treatment and etiological factors will be completely different.
Congenital heart disease may not require therapeutic measures, however, more often planned operations are performed or even urgent ones for serious, incompatible with life, inconsistencies with the norm.
Heart defects are in the class of congenital anomalies of the structure of the body in the block of anomalies of the circulatory system. VSP in ICD 10 branches into 9 sections, each of which also has subparagraphs.
However, heart problems include:
Q20 – anatomical disorders in the structure of the cardiac chambers and their connections (for example, various clefts of the oval window); Q21 – pathologies of the cardiac septum (defects of the atrial and interventricular septa and others); Q22 – problems with the pulmonary and tricuspid valves (insufficiency and stenosis); Q23 – pathologies of the aortic and mitral valves (insufficiency and stenosis); Q24 – other congenital heart defects (change in the number of chambers, dextracardia, etc.).
Each of the listed points requires further differentiation, which will allow us to determine the treatment plan and prognosis for the child. For example, with valve damage There may be symptoms of insufficiency or stenosis. In this case, the hemodynamic features of the disease will differ.
In ICD, congenital heart disease implies some kind of blood flow disturbance.
That is why in all encodings complete inversion of organs or their structures with full functioning is excluded.
Excluded: endocardial fibroelastosis (
Excludes: dextrocardia with localization inversion (Q89.3) atrial appendage isomerism (with asplenia or polysplenia) (Q20.6) mirror image of the atria with localization inversion (Q89.3)
Q24.1 Levocardia
Q24.2 Triatrial heart
Q24.3 Infundibular stenosis of the pulmonary valve
Q24.4 Congenital subaortic stenosis
Q24.5 Malformation of coronary vessels
Congenital coronary (arterial) aneurysm
Q24.6 Congenital heart block
Q24.8 Other specified congenital cardiac anomalies
Congenital: . left ventricular diverticulum. vice: . myocardium. pericardium Abnormal position of the heart Uhl's disease
Q24.9 Congenital heart defect, unspecified
Congenital: . anomaly). heart disease NOS
Congenital heart disease refers to the isolation of diseases that are combined by anatomical defects of the heart or valve apparatus. Their formation begins during the process of intrauterine development. The consequences of defects lead to disturbances in intracardiac or systemic hemodynamics.
Symptoms differ depending on the type of pathology. The most common signs are pale or blue skin, a heart murmur, and physical and mental developmental delays.
It is important to diagnose the pathology in time, since such disorders provoke the development of respiratory and heart failure.
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Congenital heart defects – ICD-10 code Q24 – include various pathologies of the cardiovascular system, accompanied by changes in blood flow. Subsequently, heart failure is often diagnosed, which leads to death.
According to statistics, every year in the world 0.8-1.2% of the total number of newborns are born with this pathology. Moreover, these defects account for about 30% of the total number of diagnosed congenital defects in fetal development.
Often the pathology in question is not the only disease. Children are also born with other developmental disorders, of which a third are musculoskeletal defects. Taken together, all the violations lead to a rather sad picture.
Congenital heart defects include the following list of defects:
ventricular or atrial septal defect; stenosis or coarctation of the aorta; pulmonary stenosis; open form of the ductus arteriosus; transposition of large great vessels.
Causes
Among the causes of this pathology in newborns, I highlight the following factors:
| Chromosomal disorders | constitute 5% of all identified cases; chromosomal aberrations often provoke the development of various intrauterine pathologies, as a result of which the child is born sick; in the case of autosomal trisomy, a defect of the interatrial and interventricular septa is formed, and abnormalities of the sex chromosomes lead to coarctation of the aorta. |
| Gene mutations | account for 2-3% of cases; the presented factor often provokes the occurrence of defects in the body’s organs; heart defects in such cases are only part of the possible dominant or recessive syndromes. |
| External factors | occupy up to 2% of all identified cases; This includes viral diseases, taking illegal drugs and harmful addictions of the mother during pregnancy, radiation and radiation, and other harmful effects on human health in general; Caution should be exercised in the first 3 months of pregnancy. |
| Rubella infection in a woman during pregnancy | This provokes glaucoma, cataracts, deafness, pathologies of the cardiovascular system, microcephaly - this disease leads to a change in the shape of the skull, resulting in a developmental delay. |
| Viral diseases | In addition to rubella, diseases such as smallpox, herpes, hepatitis, HIV infections and tuberculosis, as well as adenovirus infections, are dangerous for a woman during pregnancy. |
| Use of alcohol and illicit drugs | against the background of a woman’s alcohol addiction, the child develops a heart septal defect; amphetamines and anticonvulsants used have a negative effect; Any medications must be approved by the attending physician. |
| Diabetes and rheumatism | The likelihood of developing fetal heart disease in women with these diseases is much higher. |
The cause of pathology in newborns in the form of maternal diseases during pregnancy accounts for 90% of cases. Risk factors also include toxicosis during pregnancy in the first trimester, threats of miscarriage, genetic predisposition, endocrine system disorders and “inappropriate” age for pregnancy.
Classification
Depending on the principle of changes in hemodynamics, there is a certain classification of the presented pathology. The classification includes several types of heart disease, where the influence on pulmonary blood flow plays a key role.
| Pathologies with constant blood flow in the pulmonary circle | The variety presented includes mitral defects, stenosis and coarctation of the aorta, and other disorders. |
| Pathologies with increased blood flow | Here the defects are divided into two types depending on the possible impact on the development of cyanosis. Provoking defects include an open ductus arteriosus, childhood-type coartaction of the aorta, and others. Atresia of the tricuspid valve and other defects are expressed without consequences. |
| Pathologies with poor blood flow | There is also a division into two groups: those leading to the development of cyanosis and those not leading to such complications. |
| Combined type pathologies | Disturbances in the anatomical relationships between vessels and sections of a vital organ are determined. The presented variety includes the origin of the aorta, pulmonary trunk and other defects. |
In practice, experts divide the heart pathologies under consideration into three groups.
Here they highlight:
Hemodynamic disturbance
When these factors-causes are exposed and manifested in the fetus during development, characteristic disturbances occur in the form of incomplete or untimely closure of the membranes, underdevelopment of the ventricles and other anomalies.
Intrauterine development of the fetus is distinguished by the functioning of the ductus arteriosus and the oval window, which is in an open state. The defect is diagnosed when they still remain open.
The presented pathology is characterized by the absence of manifestations in intrauterine development. But after birth, characteristic disorders begin to appear.
Such phenomena are explained by the time of closure of the communication between the systemic and pulmonary circulation, individual characteristics and other defects. As a result, the pathology can make itself felt some time after birth.
Often, hemodynamic disorders are accompanied by respiratory infections and other concomitant diseases. For example, the presence of a pale type pathology, where arteriovenous discharge is noted, provokes the development of pulmonary hypertension, while a blue type pathology with a venoarterial shunt promotes hypoxemia.
The danger of the disease in question lies in the high mortality rate. Thus, a large discharge of blood from the pulmonary circulation, provoking heart failure, in half of the cases ends in the death of the baby before the age of one, which is preceded by the lack of timely surgical care.
The condition of a child over 1 year of age improves noticeably due to a decrease in the amount of blood entering the pulmonary circulation. But at this stage, sclerotic changes often develop in the vessels of the lungs, which gradually provokes pulmonary hypertension.
Symptoms
Symptoms appear depending on the type of anomaly, the nature and time of development of circulatory disorders. When the cyanotic form of the pathology develops in a sick child, a characteristic blueness of the skin and mucous membranes is noted, which increases its manifestation with each strain. The white defect is characterized by pallor, constantly cold hands and feet of the baby.
The baby himself with the presented disease differs from others in hyperexcitability. The baby refuses to breastfeed, and if he starts sucking, he quickly gets tired. Often, children with this pathology are diagnosed with tachycardia or arrhythmia; external manifestations include sweating, shortness of breath and pulsation of neck vessels.
In the case of a chronic disorder, the child lags behind his peers in weight, height, and there is a physical delay in development. As a rule, at the initial stage of diagnosis, a congenital heart defect is listened to, where heart rhythms are determined. In the further development of the pathology, edema, hepatomegaly and other characteristic symptoms are noted.
Complications include bacterial endocarditis, venous thrombosis, including cerebral thromboembolism, congestive pneumonia, angina syndrome and myocardial infarction.
Diagnostic measures
The disease in question is determined by using several methods of examining the child:
| Visual inspection | A specialist can determine cyanosis and its nature. Here the sign is skin tone. |
| Auscultation of the heart | Helps to identify changes in work in the form of disturbances in heart sounds, the presence of noise. A physical examination of the patient is carried out accompanied by electrocardiography, phonocardiography, radiography, and echocardiography. |
| Electrocardiography | You can identify hypertrophy of the departments and arrhythmia of the heart, characteristic conduction disturbances. The presented identified defects with additional research methods make it possible to determine the severity of the pathology. A sick child often undergoes 24-hour Holter ECG monitoring, which makes it possible to diagnose hidden disorders. |
| Phonocardiography | Necessary for determining the duration and localization of noise in a vital organ. |
| X-ray of the chest organs | It is carried out as a complement to the methods already described, which together helps to evaluate the pulmonary circulation, the size and location of internal organs and other anomalies. |
| Echocardiography | Allows you to visualize anatomical defects of the septa and valves of the heart, and allows you to determine the contractility of the myocardium. |
| Angiography and probing of some parts of the heart | Carried out for accurate diagnosis in anatomical and hemodynamic terms. |
How to treat congenital heart disease
The presented disease is complicated by performing surgery on a sick child under one year of age. Here, specialists are guided by the diagnosis of cyanotic pathologies. In other cases, operations are postponed because there is no risk of developing heart failure. Cardiology specialists work with the child.
Treatment methods and methods depend on the types and severity of the pathology in question. If an anomaly of the interatrial or interventricular septum is detected, the child undergoes plastic surgery or suturing.
In case of hypoxemia, at the initial stage of treatment, specialists perform palliative intervention, which involves the application of intersystem anastomoses. Such actions can significantly improve blood oxygenation and reduce the risk of complications, as a result of which further planned surgery will take place with favorable results.
Aortic disease is treated by resection or balloon dilatation of coarctation of the aorta, or plastic stenosis. In the case of a patent ductus arteriosus, simple ligation is performed. Pulmonary stenosis undergoes open or endovascular valvuloplasty.
If a newborn is diagnosed with a heart defect in a complicated form, where it is impossible to talk about radical surgery, specialists resort to actions to separate the arterial and venous ducts.
The anomaly itself does not disappear. It talks about the possibility of performing Fontannes, Senning and other types of operations. If surgery does not help in treatment, they resort to a heart transplant.
As for the conservative method of treatment, they resort to the use of medications, the action of which is aimed at preventing attacks of shortness of breath, acute left ventricular failure and other heart damage.
Prevention
Preventive actions for the development of this pathology in children should include careful planning of pregnancy, complete exclusion of unfavorable factors, as well as a preliminary examination to identify a risk factor.
Women who are on such an unfavorable list must undergo a comprehensive examination, which includes ultrasound and timely chorionic villus biopsy. If necessary, issues of indications for termination of pregnancy should be addressed.
If a pregnant woman is already informed about the development of pathology during fetal development, she should undergo a more thorough examination and consult with an obstetrician-gynecologist and cardiologist much more often.
Forecasts
According to statistics, mortality due to the development of congenital heart disease occupies a leading position.
In the absence of timely assistance in the form of surgical intervention, 50-75% of children die before reaching their first birthday.
Then comes a period of compensation, during which mortality rates drop to 5% of cases. It is important to identify the pathology in a timely manner - this will improve the prognosis and condition of the child.
Patent ductus arteriosus (PDA)- a vessel through which the pathological communication between the aorta and the pulmonary artery (PA) remains after birth. In healthy children, the functioning of the duct stops immediately after birth or continues in a sharply reduced volume for no more than 20 hours. Subsequently, the ductus arteriosus gradually obliterates and turns into an arterial ligament. Normally, obliteration of the duct ends in 2-8 weeks. The ductus arteriosus is considered an anomaly if it is functioning 2 weeks after birth.
Code according to the international classification of diseases ICD-10:
- P29.3
- Q21.4
- Q25.0
Statistical data: PDA is one of the most common defects (6.1% of all congenital heart defects in infants, 11-20% of all congenital heart defects diagnosed in the clinic, 9.8% according to autopsies); The ratio of male to female is 1:2.
Etiology: family cases of the defect are described; often the mother has a history of rubella, herpes, influenza at 4-8 weeks of pregnancy; Prematurity and neonatal respiratory distress syndrome, hypoxia of the newborn with a high Pg content are predisposing factors.
Pathophysiology. The direction of blood discharge is determined by the pressure difference between the aorta and the pulmonary artery and depends on the resistance value of the pulmonary and systemic vascular beds (while the pulmonary vascular resistance is lower than the systemic resistance, blood is discharged from left to right; when pulmonary resistance predominates, the direction of shunting changes). With large PDA sizes, changes in the pulmonary vessels occur early (Eisenmenger syndrome).
Symptoms (signs)
Clinical picture and diagnosis
Complaints: fatigue, shortness of breath, a feeling of interruptions in the heart, frequent infections, paradoxical embolism.
Objective examination. Retarded physical development. Pale skin, unstable cyanosis when screaming or straining. Symptoms of “drumsticks” and “watch glasses”. Persistent cyanosis when shunting blood from right to left. “Cardiac hump”, increased apical impulse, systolic tremors with a maximum in the second intercostal space to the left of the sternum. The borders of the heart are expanded to the left and right. A decrease in diastolic and an increase in pulse blood pressure, an increase in the apical impulse, an increase in both heart sounds (the volume of the second heart sound above the PA correlates with the severity of pulmonary hypertension). Rough mechanical systolic diastolic murmur in the second intercostal space to the left of the sternum, radiating into the interscapular space and to the great vessels. As pulmonary hypertension progresses and the left-to-right shunt decreases, the murmur weakens and shortens until it disappears completely (at this stage, a Graham Still diastolic murmur may appear, arising from relative insufficiency of the PA valve), followed by a repeated increase when a right-to-left shunt occurs. Sometimes above the apex of the heart there is a murmur of relative stenosis or mitral valve insufficiency.
Instrumental diagnostics
. ECG: signs of hypertrophy and overload of the right and then left parts of the heart; rarely - blockade of the His bundle branches.
. X-ray examination of the chest organs. Bulging of the PA arches, right and left ventricles. Enrichment of the pulmonary pattern, expansion and lack of structure of the roots of the lungs. Dilation of the ascending aorta. In adults, a calcified PDA can be visualized relatively rarely.
. EchoCG. Hypertrophy and dilatation of the right and left ventricles. Visualization of the PDA, determination of its shape, length and internal diameters (to assess the prognosis and select the size of the endovascular occlusion device). In the Doppler mode, a specific form of shift of the Doppler frequency spectrum in the PA is identified, the degree of shunt and the ratio of pulmonary blood flow to systemic blood flow (Qp/Qs) are determined.
. Catheterization of the left and right parts of the heart. The letter symptom is the passage of a catheter from the PA through the PDA into the descending aorta. An increase in blood oxygenation in the LA compared to the right ventricle by more than 2 volume percent. Tests with aminophylline and oxygen inhalation are performed to determine the prognosis regarding the reversibility of pulmonary hypertension.
. Ascending aortography. Receipt of contrast agent from the ascending aorta into the PA. Diagnosis of concomitant coarctation of the aorta.
Drug therapy. Before closing the PDA, prophylaxis against bacterial endocarditis is necessary. The use of indomethacin is indicated for narrow PDAs identified during the neonatal period, and is contraindicated in renal failure. Intravenous administration of indomethacin is recommended:
. less than 2 days: initial dose 200 mcg/kg; then 2 doses of 100 mcg/kg with an interval of 12-24 hours;
. 2-7 days: initial dose 200 mcg/kg; then 2 doses of 200 mcg/kg with an interval of 12-24 hours;
. more than 7 days: initial dose 200 mcg/kg; then 2 doses of 250 mcg/kg with an interval of 12-24 hours.
Treatment
Surgery
Indications. Failure of conservative therapy for 5 days or more, contraindications to the use of NSAIDs. Decompensation of circulatory failure. PDA of medium or large diameter in all children under 1 year of age.
Contraindications. Severe concomitant pathology that threatens the patient’s life. Terminal stage of circulatory failure. Irreversible pulmonary hypertension.
Methods of surgical treatment. In most cases, endovascular closure of the duct using occlusion devices (Gianturco coils, Cook coils, or umbrella devices) is feasible. If the duct is very wide or endovascular correction is unsuccessful, an open operation is performed: ligation or (less often) intersection of the PDA, followed by suturing of both ends. Thoracoscopic clipping of a PDA has no advantages over endovascular and open interventions, so it is rarely performed.
Specific postoperative complications: injury to the left recurrent laryngeal nerve, bleeding, deformation of the aorta with the formation of coarctation, residual discharge of blood through the duct due to inadequate correction.
Forecast. A narrow PDA generally does not affect life expectancy, but increases the risk of infective endocarditis. Medium and wide PDAs almost never close on their own; spontaneous closure after 3 months is rare. The effectiveness of conservative treatment of narrow PDA reaches 90%. With PDA, mortality during the first year of life is 20%. Eisenmenger syndrome in older children is observed in 14% of cases, infective endocarditis and endarteritis - in 9% of cases. Duct aneurysm and its ruptures are isolated cases. The average life expectancy for medium PDA is 40 years, for wide PDA it is 25 years. Postoperative mortality is 3%. Clinical rehabilitation, depending on hemodynamic disorders, takes place over 1-5 years.
Pregnancy. In women with a small or medium-sized PDA and left-to-right shunting, an uncomplicated course of physiological pregnancy can be expected. Women with high pulmonary resistance and a right-to-left shunt have an increased risk of complications.
Synonyms: Open botal duct; Patent ductus arteriosus; Non-closure of the ductus botallus.
Abbreviations. PDA - patent ductus arteriosus. PA - pulmonary artery.
ICD-10. P29.3 Persistent fetal circulation in the newborn. Q21.4 Defect of the septum between the aorta and pulmonary artery. Q25.0 Patent ductus arteriosus
Keywords
Dyspnea; heartbeat; cyanosis; persistent cyanosis; pulmonary; endocarditis; enterocolitis.
List of abbreviations
CHD - congenital heart defects
PA - pulmonary artery
MRI - magnetic resonance imaging
NSAIDs - non-steroidal anti-inflammatory drugs
PDA - patent ductus arteriosus
TPR - total pulmonary resistance
ECG - electrocardiography
EchoCG - echocardiography
Terms and Definitions
Cardiac catheterization is an invasive procedure performed for therapeutic or diagnostic purposes for pathology of the cardiovascular system.
Pulse pressure is the difference between systolic and diastolic pressure. Endocarditis - inflammation of the inner lining of the heart, is a common manifestation of other diseases.
Echocardiography is an ultrasound method aimed at studying the morphological and functional changes of the heart and its valve apparatus.
1. Brief information
1.1. Definition
Patent ductus arteriosus (PDA) is a vessel through which pathological communication between the aorta and the pulmonary artery (PA) remains after birth.
Comments: Normally, the PDA is necessarily present in the fetus, but closes soon after birth, turning into an arterial ligament.
1.2 Etiology and pathogenesis
Risk factors for patent ductus arteriosus are premature birth and prematurity, family history, the presence of other congenital heart diseases, infectious and somatic diseases of the pregnant woman.
1.3 Epidemiology
The exact frequency of occurrence of the defect is unknown, since it is unclear at what point a patent ductus arteriosus should be considered a pathology. It is conventionally believed that normally it should close within the first or two weeks of life. PDA usually occurs in premature infants and is extremely rare in infants born at term. Under these criteria, the incidence of isolated pathology is about 0.14-0.3/1000 live births, 7% among all congenital heart defects (CHD) and 3% among critical congenital heart defects. Persistence of the duct largely depends on the degree of term of the child: the lower the weight, the more common this pathology is.
The average life expectancy of patients with PDA is approximately 40 years. 20% of patients die before age 30, 42% before age 45, and 60% before age 60. The main causes of death are bacterial endocarditis (endarteritis), development and rupture of ductal aneurysm.
1.4 Coding according to ICD 10
Congenital anomalies of large arteries (Q25):
Q25.0 - Patent ductus arteriosus.
1.5. Classification
Taking into account the level of pressure in the pulmonary artery, 4 degrees of defect are distinguished:
The pressure in the pulmonary artery (PA) in systole does not exceed 40% of the arterial pressure;
The pressure in the PA is 40-75% of the arterial pressure (moderate pulmonary);
Pressure in the PA is more than 75% of arterial pressure (pronounced pulmonary pressure with preservation of left-right blood discharge);
The pressure in the PA is equal to or exceeds the systemic one (severe pulmonary hypertension, which leads to the occurrence of right-to-left shunting).
In the natural course of the patent ductus arteriosus there are 3 stages:
Stage I of primary adaptation (the first 2-3 years of a child’s life). Characterized by clinical manifestation of patent ductus arteriosus; often accompanied by the development of critical conditions, which in 20% of cases result in death without timely cardiac surgery.
Stage II of relative compensation (from 2-3 years to 20 years). Characterized by the development and long-term existence of pulmonary hypervolemia, relative
stenosis of the left atrioventricular orifice, systolic overload of the right ventricle.
Stage III of sclerotic changes in the pulmonary vessels. The further natural course of the patent ductus arteriosus is accompanied by a restructuring of the pulmonary capillaries and arterioles with the development of irreversible sclerotic changes in them. At this stage, the clinical manifestations of patent ductus arteriosus are gradually replaced by symptoms of pulmonary hypertension.
