Congenital heart disease (CHD) is defined as an abnormality in cardiac structure or function that is present at birth, or at times discovered much later.1, 2, 3 .The incidence of moderate to severe structural congenital heart disease is 6 to 8 per 1000 live births. 4,5-6’.This incidence had remained fairly constant over the years in different parts of the world .But in recent years there has been an increase in its incidence which may be due to the inclusion of more trivial forms of congenital heart disease, such as tiny ventricular septal defects that are detected more frequently by the use of highly sensitive echocardiography.7,8,9,10,11

CHD have a wide spectrum of severity in infants. About 2-3 / 1000 newborns will be symptomatic with heart disease in the first year of life. In 40-50% of cases the diagnosis would be established by one week and in the remaining may be diagnosed by one month of age. With improved diagnostic modalities and advances in both palliative and corrective surgery in the last two decades, the number of children diagnosed with congenital heart disease surviving to adulthood has increased dramatically.12

The timing of presentation and accompanying symptomatology may vary widely and depends on the nature and severity of the anatomic defect, the in utero effects of the structural lesions, and the alterations in cardiovascular physiology secondary to the effects of the transitional circulation.13. Signs and symptoms of heart disease in the newborn period can be variable ranging from hurried breathing, poor feeding, irritability, cyanosis, congestive heart failure, and cardiogenic shock. Rarely a baby with CHD may even be totally asymptomatic.

The presence of certain risk factors can influence the type of presentation eg; exposure to teratogens can lead to both CHD and extra cardiac manifestations.

Recognition of congenital heart disease in the newborn period is important as CHDs like Hypoplastic Left Heart Syndrome(HLHS), Coarcation Of Aorta(COA), Transpostion of Great Arteries(TGA), Total Anomalus PulmonaryVenous Connection(TAPVC) have significant mortality and morbidity in newborn period itself. These babies need to be managed on an emergency basis with medical/palliative and surgical interventions to increase their longevity.

Aim:

To determine the incidence of Congenital Heart Disease (CHD) among intramural live born neonates.

Objectives:

1. To study the clinical presentation of the neonates with CHD
2. To establish the relation between the symptoms /signs suggestive of CHD with echocardiographic finding
3. To identify the common extra cardiac manifestations associated with CHD
4. To evaluate the influence of echo cardio graphic examination in the clinical management of the sick neonate suspected to have CHD

Studies done in the last three decades indicate that the incidence of Congenital Heart Disease is increasing steadily. In 1968, Hoffmann found the incidence to be only 4-5 per 1000 live births². But, the same author in his recent study, report the incidence to be 12-14 per 1000 live births.^4,6 and other recent studies showing higher incidence up to 30|1000 live births.^8.10.11.

Bernstein et al found the relative frequency of major congenital heart diseases,

The burden of congenital heart disease in India is found to be enormous. As of now, there is no community-based data for the incidence of CHD at birth in India. Among the various hospital based studies conducted in India, the prevalence varies between 2.25 to 26.4/1000 live births3,5,15,16, the more recent ones showing a higher prevalence. This is perhaps due to increasing awareness among pediatricians who are the primary health care providers. This trend may also be related to the wide availability of trained personnel and Echocardiography machines which forms the main stay of diagnosis of CHD in neonates.3

The profile of CHD varies depending upon the age group screened. Simple and potentially correctable heart defects, like ventricular septal defect, patent ductus arteriosus and atrial septal defect, are common at all age groups.3 After studying 574 neonates, Sharma et al found VSD to be the most common Acyanotic CHD (35%), followed by PDA with 28%, and ASD 25%; in the cyanotic group, TGA was seen in one fifth of neonates with CHD and pulmonary atresia and its variants are seen in about 13% of cases.17

Even though the defect is present at birth, the age of appearance of the clinical features vary; this is because, although the most significant transitions in circulation occur in the immediate perinatal period, the circulation continues to undergo changes even after birth, and these later changes may have a hemodynamic impact on cardiac lesions. Also, the fall in pulmonary vascular resistance over the first several weeks of life, facilitates left to right shunting through intra cardiac defects which makes the symptoms more apparent. For example, in patients with a ventricular septal defect, heart failure is often manifested between one to 3 months of age.

The clinical profile of the CHDs could change as the child grows older; some ASDs and VSDs may become smaller and even close as the child grows. Alternatively, valvular defects such as stenosis of the aortic or pulmonary valve, which were mild in the newborn period, would become worse if valve orifice growth does not keep pace with patient’s growth.12

Depending upon the severity, CHD presenting at birth can be categorized into 3 groups – mild, moderate and severe categories. Severe CHD includes all cyanotic lesions and some acyanotic lesions (Large VSD, Large PDA, Critical AS, Critical PS & Critical Coarctation), which require intervention early in life. Moderate CHD (Mild- Moderate AS or PS, Non-critical Coarctation, Large ASD) are those that require expert care, but less intensive compared to severe CHD. Mild CHD (Small VSD, PDA, ASD, Mild AS or PS) are asymptomatic and often undergo spontaneous resolution.6

The risk of CHD in an offspring is 6% if mother has CHD and the risk is 3% if father has CHD,similarly when one child is born with CHD the risk for the next sibling is 3 %.18.19.

ETIOLOGY:

The etiology of CHD is complex, and in most cases multifactorial. There are a number of recognized associations like Chromosomal abnormalities (Down, Edward, Patau, Turner, Cri-du-chat) Contiguous gene syndromes (William, Di-George), Single gene defects (Noonan’s, Marfan’s, isomerism) and in addition 2- 4 % of cases of congenital heart disease are associated with known environmental or adverse maternal

conditions like congenital infection (rubella) and teratogenic drugs (anticonvulsants, lithium)12.14, 20.

TABLE   

COMMON CHROMOSOMAL ANOMALIES, SYNDROMES AND ASSOCIATED CONGENITAL HEART DEFECTS

THE NEONATE WITH CONGENITAL HEART DISEASE

An infant with cardiac disorder may present during the neonatal period in myriad ways. They can present with a constellation of symptoms ranging from breathlessness, tachycardia, bradycardia, significant murmur, poor feeding hepatomegaly or with a murmur without any symptoms. As most of these symptoms are common to many neonatal illnesses like Sepsis, RDS, Pneumonia, making a clinical diagnosis based on these symptoms alone might be difficult. Also, it is true that not all CHDs presenting in the neonatal period will have a significant murmur; so unless one has a high index of suspicion and asks for necessary investigations the diagnosis may be easily missed out. But, the presence of an abnormal facies or a syndrome like trisomies, might give a clue for a possibility of CHD.

Any infant noted to have multiple system involvement should be followed up closely for any evidence of congenital heart disease.

Age of presentation of common CHD: ²²

Congenital heart disease like TGA, Hypoplastic left heart syndrome, Aortic stenosis,Tricuspid tresia, Coarcation of aorta can present at birth while PDA,Common AVdefect manifestation around one week, Pulmonary stenosis,usually present around one month while TOFaround one year. ASD can present as late as 5 years

Congenital heart lesions presenting with shock:

Hypoplastic left heart syndrome, Interrupted aortic arch, Coarctation of aorta can present in the first week of life while myocardial disease, arrhythmias can present at any age with shock.

Congenital heart lesions presenting with asymptomatic murmur:

Congenital heart disease like Aortic stenosis, Pulmonary stenosis present in first two days of life while VSD, PDA (small) may present after 3days, ASD present usually after 3months;innocent murmurs can present at any age

SYMPTOMS AND SIGNS OF PRESENTATION OF CHD

SYMPTOMS:

Cyanosis

Hurried breathing

Excessive forehead sweating Difficulty / poor feeding Decreased urine output Convulsions, neurological deficits Not gaining weight

Irritability, restlessness

Signs

Signs of CHD include Tachypnea, Tachycardia (congestive cardiac failure), Bradycardia (heart block), Abnormal s2 - widely split and fixed S2 is seen in ASD, PS, RBBB;. a narrowly split S2 is found in conditions in which the pulmonary valve closes early (e.g., pulmonary hypertension) or the aortic valve closure is delayed (e.g., AS). The presence of Systolic murmur grade II or more Diastolic murmur Cardiomegaly, Hepatomegaly, abnormal blood pressure may also indicate the possibility of finding a structural heart disease.

BEDSIDE APPROACH TO CONGENITAL HEART

DISEASE

Criteria to Diagnose CHD - NADAS Criteria: ²³

Major criteria                                                                                 Minor criteria

Systolic murmur of > grade III                                                      Systolic murmur of < gradeIII

Diastolic murmur                                                                                Abnormal x-ray

Congestive heart failure                                                                     Abnormal ECG

Cyanosis                                                                                              Abnormal S2

abnormal blood pressure Presence of one major or two minor criteria are essential for diagnosis of heart disease.

INVESTIGATIONS IN NEONATES WITH CONGENITAL

HEART DISEASE ²⁴

Electrocardiogram

Normal ranges of QRS axis vary with age. Newborns normally have Right Axis Deviation (RAD) compared with the adult standard. Normal axis of 180° is noted in newborns (+30 to +180°). Although, in many of the CHDs, ECG may not be greatly helpful, at least certain changes are diagnostic. For example, in a cyanotic infant, left axis deviation with left ventricular hypertrophy should lead one to suspect tricuspid atresia unless proven otherwise. Rightward axis with left ventricular hypertrophy and right atrial enlargement might indicate pulmonary valve atresia/ critical pulmonic stenosis with hypoplastic right ventricle. Right axis deviation with severe right ventricular hypertrophy with very poor left ventricular voltage may mean hypoplastic left ventricle. Likewise, presence of ventricular pre-excitation of type-B in a cyanotic infant with enlarged heart might lead one to suspect Ebstein’s malformation of tricuspid valve.

Chest roentgenography

In many of the heart diseases, the ongoing hemodynamic changes could result in cardiomegaly; but, there are few exceptions. Heart is enlarged only if the cardiothoracic ratio is greater than 0.6 on the posterior-anterior view in infants. In some of the CHDs the shape of the heart may be typical. A “boot-shaped” heart with decreased pulmonary blood flow is typical in infants with cyanotic Tetralogy of Fallot (TOF), and rarely, in some infants with Tricuspid atresia too. While a narrow-waisted and “egg-shaped” heart with increased pulmonary blood flow in a cyanotic infant strongly suggests Transposition of the Great Arteries (TGA), the “snowman” sign with increased pulmonary blood flow is typical of supracardiac type of total anomalous pulmonary venous return (TAPVR); the left vertical vein, left innominate vein, and dilated SVC make up the snowman's head

2 D Echocardiography

Echocardiography (Echo) is a safe, noninvasive test for the diagnosis of CHD. provide anatomic diagnosis as well as functional information. Echo reduces the requirement for invasive studies such as cardiac catheterization. The echo examination can be used to evaluate cardiac structure in congenital heart lesions, estimate intracardiac pressures and gradients across stenotic valves and vessels, quantitate cardiac contractile function (both systolic and diastolic), determine the direction of flow across a defect, examine the integrity of the coronary arteries, and detect the presence of vegetations from endocarditis, as well as the presence of pericardial fluid, cardiac tumors, and chamber thrombi. Echocardiography may also be used to assist in the performance of pericardiocentesis, balloon atrial septostomy and endocardial biopsy and in the placement of flow-directed pulmonary artery (Swan-Ganz) monitoring catheters. A complete echocardiographic examination usually entails a combination of M-mode and two-dimensional imaging, as well as pulsed, continuous, and color Doppler flow studies.

M-MODE ECHOCARDIOGRAPHY

M-mode echocardiography displays a one-dimensional slice of cardiac structure varying over time. It is used mostly for the measurement of cardiac dimensions (wall thickness and chamber size) and cardiac function (fractional shortening, wall thickening).

DOPPLER ECHOCARDIOGRAPHY:

Doppler echocardiography displays blood flow in cardiac chambers and vascular channels based on the change in frequency imparted to a sound wave by the movement of erythrocytes

DIAGNOSTIC CARDIAC CATHETERIZION

Diagnostic catheterization is helpful to (1) to assist in the initial diagnosis of some complex congenital heart lesions (Tetralogy of Fallot with pulmonary atresia and major aortopulmonary collateral arteries [MAPCAs], pulmonary atresia with intact ventricular septum); (2) in cases in which other imaging studies are equivocal; (3) in patients for whom hemodynamic assessment is critical (to determine the size of a left- to-right shunt in borderline cases, or to determine the presence or absence of pulmonary vascular disease in a patient with a left-to-right shunt); (4) between stages of repair of complex congenital heart disease (hypoplastic left heart syndrome)

INTERVENTIONAL CARDIAC CATHETERIZATION

The miniaturization of catheter delivery systems has allowed for the safe application of many of these interventional catheterization techniques, even in neonates and premature infants.

SUBJECTS AND METHODS

The present study was conducted in a tertiary care neonatal centre between August 2011 to July 2012.During this study period all neonates who were born in the hospital suspected to have congenital heart disease formed the subjects. They were followed up to the time of discharge from nursery.

INCLUSION CRITERIA:

All intramural live born babies with clinical suspicion of congenital heart disease

EXCLUSION CRITERIA:

Out born neonates

STUDY DESIGN: Prospective observational study

BRIEF EXPLANATION OF THE PROCEDURE

Babies suspected to have CHD were included in the study .Informed consent was taken from parents of babies after explaining the nature of the study in their own language.

A clinical suspicion of CHD was entertained when babies presented with the clinical symptoms like Cyanosis ,hurried breathing, excessive forehead sweating, difficulty| poor feeding, decreased urine output, convulsions, neurological deficits, Irritability, restlessness, and signs of CHD like Tachypnea ,Tachycardia Bradycardia, Abnormal S2, Murmur and Hepatomegaly,.Those neonates who were suspected to have CHD underwent thorough general physical examination, head to foot examination for extra cardiac manifestations and also a  detailed  cardiovascular examination was done Their family history and risk factors for development of CHD were reviewed. Blood pressure was measured in all four limbs using noninvasive blood pressure (NIBP) measuring method. SpO2 was measured using Pulse Oximeter. Chest x- ray and ECG were taken initially and later an ECHO was done to confirm the diagnosis

ABG was done in needed cases. The nature of treatment given was noted down and these babies were followed up until discharged from NICCU.

STUDY DESIGN

Data Collection

A proforma was used to obtain information. The purpose of the study was explained to parents and data was collected after taking informed consent

Statistical Methods

The collected data was compiled and analyzed using MS. excel and SPSS. version 16 soft ware. Tables were generated to demonstrate the findings. Students t test, and percentage analysis was done to find p value.

Table 2. Total Number of Deliveries according to Gender and Gestation

Figure 1. Total Number of Deliveries according to Gestation and Gender

The total number of deliveries were 1819 of which 908 males (49.9%) and 911(50%) were female babies

 Total number of term deliveries 1709 in which male babies comprised of 49 % (848) and female deliveries 51 % (860). Preterm babies comprised 6 % (110)

Table 3 Gender and Gestation Wise Distribution of CHD of Cyanotic and Acyanotic Heart Disease.

In total 1819 Congenial Heart Disease (CHD) was diagnosed in 2% .Male babies were more 54%(20) while female babies comprised 46% in total CHD. .Acyanotic heart diseases comprised of 86.4% (32)while cyanotic disease 13.5%(05).

Figure- 2 showing distribution of Cyanotic and Acyanotic CHD

Table 4. Types of Congenital Heart Disease according to Gestation and Gender

8 babies were found to have multiple Congenital Heart defects.

Figure-3 showing Types of Congenital Heart Disease according to Gestation and Gender

In 37 diagnosed to have cases VSD comprised of 37% ,PDA 37% in which (Term PDA 21% preterm PDA16%) and ASD 29% while TOF, HLHS, Hypoplastic aortic arch, Dilated cardiomyopathy, PPHN, TAPVC were 2% each.

Table 5. Incidence of CHD according to Gestation

Incidence among TERM babies was 16.96|1000 live births and 7.2|1000 for PRETERM. A high significant p value (0.000) was obtained

Table6. Incidence of Cyanotic and Acyanotic CHD

Incidence of Cyanotic Heart Disease was 2.7|1000 live births and 17.5|1000 for ACYANOTIC HEART DISEASE with significant p value (0.000). TOTAL INCIDENCE OF 20.3|1000 LIVE BIRTH WAS OBTAINED FOR CONGENITAL HEART DISEASE IN THE PRESENT STUDY.

Types of acyanotic heart diseases:

Table 7. TYPES OF VENTRICULAR SEPTAL DEFECTS (VSD)

Table .8 Types of Clinical Presentation of VSD

Table 9. Gestation and Gender wise distribution of VSD

Table 10. Distribution of VSD depending on Hours of life of Clinical presentation

Table 11. Association of VSD with other heart lesion

Among Babies diagnosed as VSD, 64 % comprised of perimembranous, 28% muscular and one apical type. 78% presented after 24hrs of life and most common presentation was an asymptomatic murmur. One case presented with shock as a part of hypopastic left heart syndrome.

Table 12. Types of Atrial Septal Defect.

Table 13. Types of Clinical Presentation of ASD

Table 14. Distribution of ASD depending on Gestation and Gender

Table 15. Distribution of ASD depending on Hours of Presentation

Table 16. Association of ASD with other heart leasions

Among Babies diagnosed to have ASD, 75% comprised of ostium secondum. 66% presented after 24hrs of life. The most common presentation was an asymptomatic murmur. Two cases associated with PDA. One case was associated with TAPVC which presented as hurried respiration and cyanosis, one case presented with shock as a part of hypoplastic left heart syndrome.

Table 17. Types of Patent Ductus Arteriosus

Table 18. Types of Clinical Presentation of PDA

Table 19. Distribution of PDA depeding on Gender and Gestation

Table 20. Distribution of PDA depending on Hours of Presentation

Table 21. Association of PDA with other heart disease

Among Babies diagnosed to have PDA, 71% were small PDA. In 35% of cases the clinical presentation was a asymptomatic murmur. While 35% presented with shock, one case was associated with hypoplastic aortic arch, and two cases were preterm babies with RDS. Two cases associated with ASD.

Table 22. Clinical Presentation of suspected CHD

Figure 4 showing Clinical presentation suspected cases of CHD

Among all 61 cases suspected to have CHD 67% of cases presented as asymptomatic murmurs while 21% of cases presented as hurried respiration and or cyanosis, 12% of cases presented as shock. 34 cases presented within 24 hours with asymptomatic murmur (55%) with a significant p value (0.000). In term babies asymptomatic murmur was the most common clinical presentation. (p=0.49)

Table 23. Distribution of Cyanotic and Acyanotic CHD with Congenital Anomalies

Congenital anomalies were found in 13% of total number of CHD in the present study, Acyanotic heart disease had maximum association with congenital anomalies.

Table 24. Congenital Heart Diseases and Associated Extra cardiac Manifestations

Facial dysmorphism, cleft lip, and cleft palate were seen in two cases each .PDA had maximum associations of extracardiac anomalies.

Table 25. CONGENITAL HEART DISEASES AND CONSANGUNITY

Most common association of CHD was Acyanotic heart disease. 2 cases of ASD,and VSD and one case of PDA was associated with consagunity .Third degree consagunity was the only association.

Table 26. CLINICAL SYMPTOMS/SIGNS IN RELATION WITH ECHO

Figure- 5 showing Distribution of clinical symptoms\signs in relation with ECHO.

In babies who presented with murmurs and symptoms (20) 75% (15) were diagnosed to have CHD which was confirmed by ECHO, while in babies who had murmurs without symptoms (41) 53% had CHD confirmed by ECHO.

Table 27. IMMEDIATE OUTCOME:

37 Cases were diagnosed to have CHD in which 14 cases were advised surgery; three cases were started on antifailure measures.20 cases were told to follow-up.

A total of 1819 live babies were delivered during the study period; 908 (49.9%) were males and 911 (50.1%%) were females. 110 (6%) babies were born prematurely while the rest were term.

Of all the 1819 babies born, 37 (2%) babies were diagnosed to have Congenital Heart Disease (CHD); 32 (86.4%) babies had acyanotic CHD and only 5 babies (13.5%) had Cyanotic CHD.

Many of the cyanotic CHDs presented with respiratory distress and or cyanosis within 72 hours of life; while majority of the acyanotic CHDs were asymptomatic until discharge and were diagnosed only by the presence of a murmur. This is similar to observations made by Sharma in India and Humayun et al in Pakistan.17,25 Many of the preterm babies with PDA were symptomatic and presented early (within 24 hours) than term babies with the same disease.

Among the babies diagnosed to have CHDs, 54% were males and 46% were females; but, ASD and PDA were more common in females than males. This finding is similar to that reported in literatures. 26

The incidence of CHD in our study was 20.3 per 1000 live births. The incidence in term and preterm babies were found to be 16.96 and 7.2 per 1000 live births respectively. The incidence of acyanotic and cyanotic heart diseases were found to be

17.5 and 2.7 per 1000 live births. Both the above distributions were highly significant (p = 0.000).

Hoffmann in 2002, reported the incidence of CHD to be 4 -14 per1,000 live births. In the year 2005, another study done by Martinez et al showed an incidence of 8|1000. More recently, studies report an even more higher incidence of CHDs ranging from 18-30 per 1000 live births.6,7,8,10,11,27

Among those babies diagnosed to have CHDs, more number of babies had VSD and PDA (37% each) followed by ASD (29%). Our findings are similar to that reported by Khalil et al.15 The higher incidence of CHDs and the increased frequency of VSD and PDA seen in our study are probably due to the improved availability of manpower, increased awareness and improved diagnostic techniques, as has been already reported in literature.9

The common Cyanotic CHDs in our study were TOF (2.7%), TAPVC (2.7%), HLHS (2.7%) which was consistent with other studies15,28

Kulkarni et al in their study on 3700 consangnious couples, found CHD to be 10 times more common in babies born to them, than those born to non-consangnious couples; similar observation were made by other authors; .30.31,32however, in our study, Consangunity (third degree) was seen in only 13% of the diagnosed CHDs.

In a Danish study32 the risk of CHD in singleton births with first-, second-, or third-degree relatives with CHD was 3.2 (95% CI 3.0-3.5), 1.8 (95% CI 1.1-2.9), or 1.1 (95% CI 0.8-1.5), respectively. But, we did not find similar observation in our study.

All the babies diagnosed to have CHD in our study, had some murmur; and it is this murmur that made us to suspect CHD in them. This is similar to the observation made by Ivan et al in Brazil. 33.

Khalil15 and shamima29 have observed breathing difficulty and cyanosis as the most common presentations of CHD babies than asymptomatic murmur. Even though, we also have observed hurried respiration and cyanosis as the common presenting symptoms in those who are symptomatic, asymptomatic murmur was much more common (67%) than those with symptoms.

Among 61 babies suspected to have CHD, based on the presence of a murmur, 34 of them (64%) were diagnosed within 24 hours which was statistically significant

(p value 0.000).

In those babies who had symptoms in addition to murmur, the number of ECHO proved CHDs were found to be high (75%) compared to those babies who presented with asymptomatic murmur (53%).

Kadivar et al28 in a study of sick neonates observed a change in the clinical management in at least 66% of newborns scanned, including emergency surgical intervention for 7%, medical treatment for 22%, and routine cardiologic follow-up for 37% of patients. Moss et al34 showed that Echo prompted a specific change in clinical management in (78%) babies. Similar results were shown by Wren et al35 and Anisworth36 which signifies the influence of ECHO in management of sick neonates. In our study also, in atleast 37% of babies diagnosed to have CHD by Echocardiogram, it helped us in early decisions in initiating the management or early referral for those who needed immediate surgical intervention.

In the present study, 13% of the babies with CHD were found to have some extra-cardiac malformations; this is slightly less when compared to those reported in other studies37

Incidence of Congenital heart disease is high in our study-20.3/live birth

VSD and PDA are the commonest CHDs.

Symptomatic murmur had a higher yield of CHD on echocardiogram.

Clinical follow-up is needed for babies who presented with murmurs without symptoms.

Early diagnosis by combined clinical examination and Echocardiography helps in planning effective treatment thereby reducing morbidity and mortality.

LIMITATIONS OF OUR STUDY:

Only short-term outcome was studied

No data regarding outcome of babies who were referred for surgery.

Follow-up data regarding asymptomatic babies were not included in the study as it was not an objective of the study.

SUGGESTIONS FOR FURTHER STUDIES

A prospective longitudinal multicentric can be done to follow-up all babies with clinical suspicion of CHD to find out both short term as well as long term outcomes in them.

Genetic studies can be undertaken to find out probable mutations that result in CHD

The role of prenatal diagnosis in CHD can be studied.

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