Transposition of the great vessels

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Cafer Zorkun, M.D., Ph.D. [3]; Keri Shafer, M.D. [4]; Kristin Feeney, B.S. [5]

Transposition of the great arteries (TGA) is a pediatric cardiac congenital defect arising from an embryological discordance between the aorta and pulmonary trunk. During cardiac development, the conotruncal septum spirals toward the aortic sac thus dividing the truncus arteriosus into the pulmonary and aortic channels. These channels then become the pulmonary arteries and aorta, respectively. TGA occurs when the conotruncal septum fails to follow its spiral course and instead forms in a linear orientation. Consequently, the aorta arises from the right ventricle and the pulmonary trunk arises from the left ventricle. The TGA was first described in 1797 by Matthew Baillie as a “singular malformation”. The word transposition was coined by Farre in 1814. Right atrium (RA) is connected to a morphologic right ventricle (RV). The morphologic left atrium (LA) is connected to the morphologic left ventricle (LV). This is called atrio-ventricular concordance. In a normal heart, the great arteries (aorta and pulmonary arteries) are concordant with the morphologic LV and RV. This is termed ventriculo-arterial concordance. In addition, the aorta and pulmonary trunk ascend in a spiral relationship. In the TGA the aorta arises from the morphologic right ventricle via a subaortic infundibulum and the pulmonary artery arises from the morphologic left ventricle, without a subpulmonary infundibulum. These ventriculoarterial connection is known as ventriculoarterial discordance. The abnormal origin of the great arteries results in an altered spiral relationship resulting in parallel circulation. Transposition of great vessels can be classified based on concordance of ventriclular positions into dextro-TGA and levo-TGA. The causes for transposition of the great arteries is unknown and is presumed to be multifactorial. The embryology likely involves abnormal persistence of the subaortic conus with resorption or underdevelopment of the subpulmonary conus (infundibulum). This abnormality aligns the aorta anterior and superior with the right ventricle during development. The prevalence of TPA is approximately 47 per 100,000 individuals worldwide. TGA accounts for 5-7 percent of all congenital heart disease and 20 percent of cyanotic heart disease. There is no racial predilection to transposition of great vessels. Transposition of the great arteries has a 60-70% male predominance. TGA is not known to be associated with any specific single gene defect, but some studies have shown possible genetic association in some cases of TGA, involving deletions of chromosome 22q11. Other risk factors in the mother that may increase the risk of this condition include age over 40, alcoholism, diabetes, prenatal malnutrition and rubella or other viral illness during pregnancy. Majority of the time, diagnosis can be made after 18 weeks gestation using an ultrasound. However, if it is not diagnosed in utero, cyanosis of the newborn should immediately direct towards diagnosis of TGA. If left untreated, over 50 percent of infants with transposition of the great arteries will die in the first month of life. 90 percent will die in the first year. Common complications of TGA include congestive heart failure, arrhythmia, pulmonary artery stenosis and aortic regurgitation. The prognosis for patients with TGA is generally excellent following surgical correction with survival rates greater than 90%. Without treatment, 30% of infants die within the first week of life, 50% will die in the first month, 70% will die in the first 6 months and 90% of infants will die before the end of the first year. The clinical features of D-TGA are solely dependent on the degree of mixing between the parallel circuits. Most patients present with signs and symptoms during the neonatal period. Symptoms of D-TGA present with cyanosis, tachypnea and murmurs. Patients with L-TGA present with symptoms of heart failure until later in life when the right ventricle can no longer compensate increased after load. Newborns with transposition of the great arteries are usually well developed, without dysmorphic features. Physical findings at presentation depend on the presence of associated lesions. In many cases, TGV is accompanied by other heart defects, the most common type being intracardiac shunts such as atrial septal defect (ASD), patent foramen ovale (PFO), ventricular septal defect (VSD), and patent ductus arteriosus (PDA). Stenosis, or other defects, of valves and/or vessels may also be present. An abnormal pulse oximetry findings with a discrepancy between the upper and lower extremities is a consistent finding with transposition of great vessels. D-TGA is difficult to detect on fetal ultrasound due to the absence of differences in ventricle size. There are no specific ECG findings associated with TGA. However, sometimes electrocardiogram may show right axis deviation and right ventricular hypertrophy. An x-ray may be helpful in the diagnosis of TGA. Findings on an x-ray suggestive of TGA include egg on a string appearance of the heart, increased pulmonary vascular markings, and cardiomegaly. Echocardiography and Doppler examination acts as the main diagnostic tool in transposition of great artyeries. Echocardiography demonstrates pulmonary arteries arising from the posterior left ventricle, and the aorta rising anteriorly from the right ventricle. Echocardiography also detects other associated anomalies like ventricular septal defect (VSD), patent ductus arteriosus and the coronary artery anatomy. Computed tomography can be helpful as a diagnostic tool in conditions where the echocardiographic findings are inconclusive. CT can done faster compared to MRI, thus avoiding the need for anesthesia in small children. Provides additional anatomic details compared to echocardiography. Magnetic resonance imaging (MRI) can be used as a diagnostic modality in congenital heart diseases. Helps in measuring heart volumes, blood flow and ventricular wall thickness. MRI can be used in cases where echocardiographic results are inconclusive. Cardiac catheterization is not frequently done to diagnose transposition of the great vessels, as it could be done confidently with echocardiography. It is in conditions when the echo findings are inconclusive. It can be used to determine the coronary anatomy. Cardiac catheterization can also be used as interventional while performing balloon atrial septostomy. This operation helps to increase mixing between the two circulatory systems. Surgery is the mainstay of treatment for TGA. However, infusion of PGE1 to a newborn diagnosed with TGA is recommended as it prevents the ductus arteriosus from closing, therefore providing an additional shunt through which to provide the systemic circulation with a higher level of oxygen. Surgical approach is the mainstay of treatment for transposition of great vessels. Type of surgery mainly depends on the age of the patient at presentation, the presence of associated congenital cardiac lesions, and the experience of the cardiothoracic surgeon with a given surgical technique. Most full-term neonates with uncomplicated transposition of the great arteries can undergo an arterial switch procedure in one operation, with minimal mortality. Recent advances in surgical correction of transposition of the great arteries have reduced the mortality drastically from 95% in uncorrected patients to 5% in corrected patients. Post-operative care is very similar to the palliative care received, with the exception that the patient no longer requires PGE or the surgical palliation procedures. Additionally, the patient is kept on a cooling blanket for a period of time to prevent fever, which could cause brain damage. The sternum is not closed immediately which allows extra space in the thoracic cavity, preventing excess pressure on the heart, which swells considerably following the surgery; the sternum and incision are closed after a few days, when swelling is sufficiently reduced.

The TGA was first described in 1797 by Matthew Baillie as a “singular malformation”. The word transposition was coined by Farre in 1814.

Transposition of great vessels can be classified based on concordance of ventriclular positions into dextro-TGA and levo-TGA.

Right atrium (RA) is connected to a morphologic right ventricle (RV). The morphologic left atrium (LA) is connected to the morphologic left ventricle (LV). This is called atrio-ventricular concordance. In a normal heart, the great arteries (aorta and pulmonary arteries) are concordant with the morphologic LV and RV. This is termed ventriculo-arterial concordance. In addition, the aorta and pulmonary trunk ascend in a spiral relationship. In the TGA the aorta arises from the morphologic right ventricle via a subaortic infundibulum and the pulmonary artery arises from the morphologic left ventricle, without a subpulmonary infundibulum. These ventriculoarterial connection is known as ventriculoarterial discordance. The abnormal origin of the great arteries results in an altered spiral relationship resulting in parallel circulation.

The causes for transposition of the great arteries is unknown and is presumed to be multifactorial. The embryology likely involves abnormal persistence of the subaortic conus with resorption or underdevelopment of the subpulmonary conus (infundibulum). This abnormality aligns the aorta anterior and superior with the right ventricle during development.

The prevalence of TPA is approximately 47 per 100,000 individuals worldwide. TGA accounts for 5-7 percent of all congenital heart disease and 20 percent of cyanotic heart disease. There is no racial predilection to transposition of great vessels. Transposition of the great arteries has a 60-70% male predominance.

TGA is not known to be associated with any specific single gene defect, but some studies have shown possible genetic association in some cases of TGA, involving deletions of chromosome 22q11. Other risk factors in the mother that may increase the risk of this condition include age over 40, alcoholism, diabetes, prenatal malnutrition and rubella or other viral illness during pregnancy.

Majority of the time, diagnosis can be made after 18 weeks gestation using an ultrasound. However, if it is not diagnosed in utero, cyanosis of the newborn should immediately direct towards diagnosis of TGA.

If left untreated, over 50 percent of infants with transposition of the great arteries will die in the first month of life. 90 percent will die in the first year. Common complications of TGA include congestive heart failure, arrhythmia, pulmonary artery stenosis and aortic regurgitation. The prognosis for patients with TGA is generally excellent following surgical correction with survival rates greater than 90%. Without treatment, 30% of infants die within the first week of life, 50% will die in the first month, 70% will die in the first 6 months and 90% of infants will die before the end of the first year.

The clinical features of D-TGA are solely dependent on the degree of mixing between the parallel circuits. Most patients present with signs and symptoms during the neonatal period. Symptoms of D-TGA present with cyanosis, tachypnea and murmurs. Patients with L-TGA present with symptoms of heart failure until later in life when the right ventricle can no longer compensate increased after load.

Newborns with transposition of the great arteries are usually well developed, without dysmorphic features. Physical findings at presentation depend on the presence of associated lesions. In many cases, TGV is accompanied by other heart defects, the most common type being intracardiac shunts such as atrial septal defect (ASD), patent foramen ovale (PFO), ventricular septal defect (VSD), and patent ductus arteriosus (PDA). Stenosis, or other defects, of valves and/or vessels may also be present.

An abnormal pulse oximetry findings with a discrepancy between the upper and lower extremities is a consistent finding with transposition of great vessels. D-TGA is difficult to detect on fetal ultrasound due to the absence of differences in ventricle size.

There are no specific ECG findings associated with TGA. However, sometimes electrocardiogram may show right axis deviation and right ventricular hypertrophy.

An x-ray may be helpful in the diagnosis of TGA. Findings on an x-ray suggestive of TGA include egg on a string appearance of the heart, increased pulmonary vascular markings, and cardiomegaly.

Echocardiography and Doppler examination acts as the main diagnostic tool in transposition of great artyeries. Echocardiography demonstrates pulmonary arteries arising from the posterior left ventricle, and the aorta rising anteriorly from the right ventricle. Echocardiography also detects other associated anomalies like ventricular septal defect (VSD), patent ductus arteriosus and the coronary artery anatomy.

Computed tomography can be helpful as a diagnostic tool in conditions where the echocardiographic findings are inconclusive. CT can done faster compared to MRI, thus avoiding the need for anesthesia in small children. Provides additional anatomic details compared to echocardiography.

Magnetic resonance imaging (MRI) can be used as a diagnostic modality in congenital heart diseases. Helps in measuring heart volumes, blood flow and ventricular wall thickness. MRI can be used in cases where echocardiographic results are inconclusive.

Cardiac catheterization is not frequently done to diagnose transposition of the great vessels, as it could be done confidently with echocardiography. It is in conditions when the echo findings are inconclusive. It can be used to determine the coronary anatomy. Cardiac catheterization can also be used as interventional while performing balloon atrial septostomy. This operation helps to increase mixing between the two circulatory systems.

Surgery is the mainstay of treatment for TGA. However, infusion of PGE1 to a newborn diagnosed with TGA is recommended as it prevents the ductus arteriosus from closing, therefore providing an additional shunt through which to provide the systemic circulation with a higher level of oxygen.

Surgical approach is the mainstay of treatment for transposition of great vessels. Type of surgery mainly depends on the age of the patient at presentation, the presence of associated congenital cardiac lesions, and the experience of the cardiothoracic surgeon with a given surgical technique. Most full-term neonates with uncomplicated transposition of the great arteries can undergo an arterial switch procedure in one operation, with minimal mortality. Recent advances in surgical correction of transposition of the great arteries have reduced the mortality drastically from 95% in uncorrected patients to 5% in corrected patients.

Post-operative care is very similar to the palliative care received, with the exception that the patient no longer requires PGE or the surgical palliation procedures. Additionally, the patient is kept on a cooling blanket for a period of time to prevent fever, which could cause brain damage. The sternum is not closed immediately which allows extra space in the thoracic cavity, preventing excess pressure on the heart, which swells considerably following the surgery; the sternum and incision are closed after a few days, when swelling is sufficiently reduced.

The development of a fetal heart starts during the first trimester of pregnancy. Thus, many a times the fetal heart has already developed, by the time the female becomes aware of being pregnant. There are some risk factors that if avoided before and during pregnancy can decrease the occurrence of congenital heart diseases.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Cafer Zorkun, M.D., Ph.D. [3]; Keri Shafer, M.D. [4]; Kristin Feeney, B.S. [5]

The TGA was first described in 1797 by Matthew Baillie as a “singular malformation”. The word transposition was coined by Farre in 1814.

• The TGA was first described in 1797 by Matthew Baillie as a “singular malformation”.^[1][2][3][4]
• In 1814 Farre described it as transposition.
• No treatment was available until the middle of the 20th century.
• In the 1950s, surgical atrial septectomy was developed followed by balloon atrial septostomy in the 1960s. These surgical therapies were not curative, but were palliative. They were later followed by physiological procedures.
• Today, the survival rate for infants with TGA is greater than 90%.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Cafer Zorkun, M.D., Ph.D. [3]; Keri Shafer, M.D. [4]; Kristin Feeney, B.S. [5]

Right atrium (RA) is connected to a morphologic right ventricle (RV). The morphologic left atrium (LA) is connected to the morphologic left ventricle (LV). This is called atrio-ventricular concordance. In a normal heart, the great arteries (aorta and pulmonary arteries) are concordant with the morphologic LV and RV. This is termed ventriculo-arterial concordance. In addition, the aorta and pulmonary trunk ascend in a spiral relationship. In the TGA the aorta arises from the morphologic right ventricle via a subaortic infundibulum and the pulmonary artery arises from the morphologic left ventricle, without a subpulmonary infundibulum. These ventriculoarterial connection is known as ventriculoarterial discordance. The abnormal origin of the great arteries results in an altered spiral relationship resulting in parallel circulation.

• In the fifth week of gestation, opposing pairs of ridges form in the truncus arteriosus.^[1][2][3]
• These ridges are termed the right superior truncus swelling and the left inferior truncus swelling.
• The right superior truncus swelling grows distally and to the left while the left inferior truncus swelling grows distally and to the right.
• The result is twisting of the swellings around each other and the foreshadowing of the anatomically normal spiral septum.  
• Simultaneously, swellings in the dorsal and ventral walls of the conus cordis appear and grow toward each other and distally.
• Eventually, these swellings fuse with each other, as well as the truncus septum, thus dividing the conus cordis into anterolateral (right ventricular outflow tract) and posteromedial (left ventricular outflow tract) portions.
• Equally important to septal formation, is the migration of neural crest cells through pharyngeal arches three, four, and six, and to the heart.
• There, they contribute to endocardial cushion formation in the truncus arteriosus and conus cordis, as well as lengthening of the outflow tracts.
• Any insult to the migration of neural crest cells can cause tetralogy of Fallot, truncus arteriosus, and TGA.

Normal Heart

• Right atrium (RA) is connected to a morphologic right ventricle (RV).
  • The morphologic left atrium (LA) is connected to the morphologic left ventricle (LV). This is called atrio-ventricular concordance.
• In a normal heart, the great arteries (aorta and pulmonary arteries) are concordant with the morphologic LV and RV.
  • This is termed ventriculo-arterial concordance.
• In addition, the aorta and pulmonary trunk ascend in a spiral relationship.

Transposition of the great vessels

• In the TGA the aorta arises from the morphologic right ventricle via a subaortic infundibulum and the pulmonary artery arises from the morphologic left ventricle, without a subpulmonary infundibulum.
• These ventriculoarterial connection is known as ventriculoarterial discordance.
• As a consequence, there is a a fibrous continuity between the mitral and pulmonary valve, but no continuity between the tricuspid and aortic valve.
• The abnormal origin of the great arteries results in an altered spiral relationship.
• Therefore, the aorta and pulmonary artery run parallel to each other
• In normal heart thus the circulation is in series.
• However, in transposition of the great vessels circulation is in parallel

• The fetus circulation in-utero is different compared to the extra-uterine circulation.^[4]
• The fetus tolerates a D-TGA well in-utero due to this difference in circulation.
• The high resistance in the pulmonary circulation compared to the placenta, allows the blood to flow to the descending aorta rather than to the lung.
• Due to this the fetus gets blood with a higher oxygen tension.

• Fetal Ciculation→Oxygen-rich blood from placenta(drains to)→Umbilical vein (drains to)→Right atrium (drains to) →Fossa ovalis(drains to)→Left ventricle (drains to)→The pulmonary artery(drains to)→Ductus arteriosus(drains to)→Descending aorta.Pathophysiology in Dextro-TGA in extra-uterine life–

• In normal cardiac anatomy, the aorta is positioned posterior and to the right of the main pulmonary artery.
• Aorta being positioned anterior and slightly rightward of the pulmonary artery.
• These changes cause the aorta to arise from the right ventricle and the pulmonary artery from the left ventricle (ventriculoarterial discordance).
• In Uncorrected D-TGA the systemic and pulmonary circulations are parallel circuits which means that the deoxygenated systemic venous blood comes to the right ventricle and inplace of going to the lungs, drains back to the systemic circulation via the aorta.
• Similarly, oxygenated pulmonary venous blood is recirculated to the lungs via the pulmonary artery.
• This parallel circulation is incompatible to life.
• For a child with dextro-TGA to survive, a communication between the two parallel circuits is necessary.
• Various connections that allow mixing in these patients are: patent foramen ovale, ventricular septal defect, atrial septal defect,patent ductus arteriosus or the bronchopulmonary collateral circulation.
  • Ventricular septal defect (VSD) occurs (in about 50%) of patients with D-TGA. Patients with a VSD may have other cardiac anomalies like pulmonary stenosis or atresia, overriding of atrioventricular valve, and coarctation of aorta.
  • Left ventricular outflow tract obstruction is common in D-TGA and is present in up to 25 percent of patients.

Below is an image depicting the abnormal flow in the large vessels of the heart.

• Levo-TGA (L-TGA) is a lesser known form of TGA.
• The left ventricle is positioned to the right of the right ventricle (opposite sides of the heart).
• The pulmonary trunk and aorta arise in their anatomically correct orientations, however, since the ventricles are reversed, the aorta is fused with the right ventricle, and the pulmonary trunk is combined with the left ventricle.
• The resultant flow of blood in a patient with L-TGA is as follows:
  • Deoxygenated blood enters the anatomically correct right atrium, passes through the mitral valve into the left ventricle, and is pumped into the pulmonary trunk to the lungs.
  • From the lungs, the oxygenated blood enters the left atrium, passes through the tricuspid valve, and into the right ventricle where blood is then pumped into the aorta.
  • Since the flow of blood in patients with L-TGA passes through the normal systemic and pulmonary circuits, L-TGA is sometimes termed anatomically correct TGA.

Conditions associated with TGA include:

• Ventricular septal defect
• Pulmonary stenosis
• Left atrioventricular valve regurgitation (tricuspid or systemic)
• Complete heart block

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Cafer Zorkun, M.D., Ph.D. [3]; Keri Shafer, M.D. [4];Kristin Feeney, B.S. [5]

The causes for transposition of the great arteries is unknown and is presumed to be multifactorial. The embryology likely involves abnormal persistence of the subaortic conus with resorption or underdevelopment of the subpulmonary conus (infundibulum). This abnormality aligns the aorta anterior and superior with the right ventricle during development.

• The etiology for transposition of the great arteries is unknown and is presumed to be multifactorial.^[1]
• The embryology likely involves abnormal persistence of the subaortic conus with resorption or underdevelopment of the infundibulum. This abnormality aligns the aorta anterior and superior with the right ventricle during development.
• Generally, TGA is not known to be associated with any specific single gene defect, but some studies have shown possible genetic association in some cases of TGA, involving deletions of chromosome 22q11.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Cafer Zorkun, M.D., Ph.D. [3]; Keri Shafer, M.D. [4]; Assistant Editor(s)-In-Chief: Kristin Feeney, B.S. [5]

Patients with transposition of the great vessels should be differentiated from other cardiac and non-cardiac causes of cyanosis.

Patients with transposition of the great vessels should be differentiated from other cardiac and non-cardiac causes of cyanosis-

Cardiac causes (starts with ‘t’)-

• Tetralogy of Fallot
• Truncus arteriosus
• Total anomalous pulmonary venous connection
• Tricuspid valve abnormalities

Other less common causes are- pulmonary atresia, hypoplastic left heart syndrome, anomalous systemic venous connection.

Non-cardiac causes

• Pulmonary diseases – Structural abnormalities of the lung, V/P (ventilation-perfusion mismatch), airway obstruction, pneumothorax, and hypoventilation.
• Abnormal hemoglobin like methemoglobin, polycythemia
• Peripheral cyanosis for e.g. sepsis, hypoglycemia, dehydration, and hypoadrenalism.

Transposition of the great arteries should be differentiated from other cyanotic congenital heart diseases found in the pediatrics population. These disorders described in the table below:

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Cafer Zorkun, M.D., Ph.D. [3]; Keri Shafer, M.D. [4]; Kristin Feeney, B.S. [5]

The prevalence of TPA is approximately 47 per 100,000 individuals worldwide. TGA accounts for 5-7 percent of all congenital heart disease and 20 percent of cyanotic heart disease. There is no racial predilection to transposition of great vessels. Transposition of the great arteries has a 60-70% male predominance.

• Transposition of the great arteries TGA is one of the commonest cyanotic congenital heart defects present in the first 24 hours of life.^[1]
• The overall annual incidence of TGA is 20-30 per 100,000 live births.
• TGA represents 5-7% of all congenital heart disease and 20% of cyanotic disease.

• Boys outnumber girls with an approximate ratio of 2:1.

• There is no racial predilection to transposition of great vessels.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Cafer Zorkun, M.D., Ph.D. [3]; Keri Shafer, M.D. [4]; Kristin Feeney, B.S. [5] Aditya Ganti M.B.B.S. [6]

TGA is not known to be associated with any specific single gene defect, but some studies have shown possible genetic association in some cases of TGA, involving deletions of chromosome 22q11. Other risk factors in the mother that may increase the risk of this condition include age over 40, alcoholism, diabetes, prenatal malnutrition and rubella or other viral illness during pregnancy.

Generally, TGA is not known to be associated with any specific single gene defect, but some studies have shown possible genetic association in some cases of TGA, involving deletions of chromosome 22q11. Other risk factors in the mother that may increase the risk of this condition include:

• Age over 40
• Alcoholism
• Diabetes^[1]
• Prenatal malnutrition
• Rubella or other viral illness during pregnancy^[2]
• Maternal use of anti eplileptic drugs^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Cafer Zorkun, M.D., Ph.D. [3]; Keri Shafer, M.D. [4]; Kristin Feeney, B.S. [5]

Majority of the time, diagnosis can be made after 18 weeks gestation using an ultrasound. However, if it is not diagnosed in utero, cyanosis of the newborn should immediately direct towards diagnosis of TGA.

Majority of the time, diagnosis can be made after 18 weeks gestation using an ultrasound. However, if it is not diagnosed in utero, cyanosis of the newborn should immediately direct towards diagnosis of TGA.^[1]

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