TGA-Dr.Elamaran
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Transcript of TGA-Dr.Elamaran
Dr.Elamaran.E
Senior Resident Dept. of CTVS,JIPMER
o Congenital cardiac anomaly
o Atrioventricular concordance and Ventriculo arterial discordance.
o Aorta arises from the morphologic right ventricle and the pulmonary artery arises from the morphologic left ventricle.
Morphologic description of TGA –Baillie(1797)
Transposition of the aorta and pulmonary artery was coined - Farre (1814)
Surgery for TGA Atrial septectomy - Blalock and
Hanlon(1950) Balloon atrial septostomy - Rashkind
and Miller - (1966)
Partial physiological correction – Lillehei (1953)
Physiologic correction at the atrial level –Senning(1959) and Mustard(1963)
Arterial switch procedure –Jatene (1975)
Etiology for transposition of the great arteries is unknown and is presumed to be multifactorial.
Common association in infants of diabetic mothers.
Persistence of sub Aortic conus and absorption of sub pulmonary conus
Failure of the Truncus Arteriosus to septate normally
Transposition of the great arteries (TGA) is the most common cyanotic congenital heart lesion that presents in neonates.
This lesion presents in 5-7% of all patients with congenital heart disease.
Male-to-female ratio is 2:1. Male predominance increases to 3.3 : 1 (ventricular septum is intact)
Right ventricle –Hypertrophied, Sub aortic conusLeft ventricle- Normal to thinned out, Pulmonary-Mitral continuityAorta- Anterior and right of PAAtria – Normal (RA>LA)Atrio-Ventricular valves – Same levelConduction tissue – Normal position and abnormal shape
Normal -2/3 and Abnormal -1/3
The pulmonary and systemic circulations function in parallel, rather than in series.
When patients with all varieties of TGA are considered
55% - 1 month 15% - 6 months 10% - 1 year
Transposition of the great arteries with intact ventricular septum – Hypoxia
Transposition of the great arteries with ventricular septal defect –cardiac failure
Transposition of the great arteries with ventricular septal defect and left ventricular outflow tract obstruction- Hypoxia
Aggressive medical and surgical management in the neonate has around 90% early and midterm survival
1. TGA with intact ventricular septum
2. TGA with VSD
3. TGA with VSD and LVOTO
4. TGA with VSD and pulmonary vascular obstructive disease.
Patent foramen ovale or Atrial septal defect- 75%
Ventricular septal defect- 25% -40% Patent ductus Arteriosus-functionally
closes by 1 month Left ventricular outflow obstruction-5% Mitral valve-cleft leaflet/accessory
chordal tissue Tricuspid valve – regurgitation/dysplasia
Symptoms and clinical presentation
Depend on degree of mixing between the two parallel circulatory circuits.
TGA with intact ventricular septum – Cyanosis within 24 hours
TGA with VSD– congestive heart failure (2 to 4 months)
TGA with VSD and LVOTO- similar to TOF
TGA with VSD and PVOD – develop Hypoxia after 6 months
An oval-or egg-shaped cardiac silhouette with a narrow superior mediastinum
Mild cardiac enlargement
Moderate pulmonary plethora
Simple TGA – Neonates- Arterial switch within 1 month
Simple TGA – after 30 days Pulmonary artery banding- Arterial
switch after 2 weeks Atrial switch
TGA with VSD- Arterial switch within few weeks
TGA with VSD and LVOTO – repair - 6 months
Establishing Ventriculo-arterial concordance
Anatomical correction
Coronary artery lesions
Neo Aortic valve regurgitation
RVOTO and LVOTO obstruction
Cardiac failure- Secondary to severe LV dysfunction(imperfect coronary artery transfer to Neoaorta)
RV dysfunction – Progressive pulmonary vascular disease (1%)
Coronary events
Physiological correction
Baffle obstruction and leak
Rhythm disturbances
Severe Tricuspid regurgitation
Right ventricle failure
Low output – early post op period
Systemic RV failure
Aortic translocation(TGA with VSD & LVOTO) – Nikaidoh
Damus-Kaye-Stansel(TGA with large VSD and RVOTO)
TGA with posterior Aorta- Arterial switch procedure without Lecompte maneuver
Thank You