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The first total repair of tetralogy of Fallot was done by a team led by C. Walton Lillehei at the University of Minnesota in 1954 on an 11-year-old boy. [85] Total repair on infants has had success from 1981, with research indicating that it has a comparatively low mortality rate. [ 72 ]
A diagnosis of TOF is usually made with echocardiography, which can even be done prenatally. Most patients with tetralogy of Fallot will have cardiac repair surgery in the first year of life, where the ventricular septal defect is closed with a patch, and the right ventricular outflow tract is enlarged.
Without treatment, it is a highly life-threatening condition, so prognosis is poor. [35] [34] If surgery isn't performed in severe cases, the child can (and will) die, since the phenotype of pulmonary atresia is not compatible with life due to the pulmonary valve atresia resulting in reduced blood oxygenation. [9] [62] [63]
Digital clubbing with cyanotic nail beds in an adult with tetralogy of Fallot. Signs and symptoms are related to type and severity of the heart defect. Symptoms frequently present early in life, but it is possible for some CHDs to go undetected throughout life. [15]
The Blalock–Thomas–Taussig shunt (BTT shunt), [1] previously known as the Blalock–Taussig Shunt (BT shunt), [2] is a surgical procedure used to increase blood flow to the lungs in some forms of congenital heart disease [3] such as pulmonary atresia and tetralogy of Fallot, which are common causes of blue baby syndrome. [3]
Taussig–Bing syndrome is a cyanotic congenital heart defect [1] in which the patient has both double outlet right ventricle (DORV) and subpulmonic ventricular septal defect (VSD).
All infants with TGA will need surgery to correct the defect. Life expectancy is only a few months if corrective surgery is not performed. [citation needed] Before surgery: For newborns with transposition, prostaglandins can be given to keep the ductus arteriosus open which allows for the mixing of the otherwise isolated pulmonary and systemic ...
The most typical form of APVS is a tetralogy of Fallot variant, [4] however, case studies have linked APVS to several different congenital cardiac syndromes, such as agenesis of ductus arteriosus, [5] persistent ductus arteriosus, [6] atrioventricular septal defect, [7] pulmonary branching abnormalities, [8] [9] transposition of the great arteries, [10] and type B interrupted aortic arch. [11]