User:ShaoniD/Helen B. Taussig

Blue Baby syndrome- not getting enough oxygen

resulted as a consequence of the closure of the ductus arteriosus, which allows the blood in the heart to be directly transferred from the pulmonary arteries to the aorta as a fetus. The lungs have not fully developed yet in the fetus and most of the oxygen is obtained from the mother's placenta

Early Life and Career (continuation of original)
Helen. B Taussig attended Harvard's School of Public Health, though she aspired to be a physician. At the time, women were not allowed to obtain a degree in medicine from Harvard, so Taussig attended Boston University's School of Medicine. There, with the encouragement of her professor Alexander Begg, she decided to pursue further studies into the heart. Begg also aided her acceptance into Johns Hopkins School of Medicine.

In 1930, Helen B. Taussig became the head of the Harriet Lane Home, a Pediatric Cardiac Clinic. She fulfilled her duties as the head until 1963 when she retired.

During her early career she studied babies with congenital heart defects as well as rheumatic fever. The latter is a consequence of streptococcus infection. This interest eventually led to her finding a possible method of treatment for "Blue Baby Syndrome."

After proposing the idea to Alfred Blalock, the team consisting of Taussig, Blalock, and Thomas, experimented the procedure on around 200 dogs. Then Taussig received a severely affected patient, who received the first trial of the procedure: Eileen Saxon. Saxon was believed to be a textbook case of the "Blue Baby Syndrome" with apparent features, such as a tinge in blue lips. The procedure itself was successful. However, Saxon contrived recurrent stenosis, which deteriorated her condition and ultimately lead to her fatality.

Taussig Collaborations
The collaboration that Taussig is primarily known for is that with Alfred Blalock in inventing a technique for the Blue Baby Syndrome. However, throughout her career, Taussig has collaborated with other physicians as well.

Of the many advancements in Taussig's career, she was known to be the director of the Harriet Lane Home facility, or a Pediatric Cardiac Center. Helen B. Taussig succeeded Clifton Briggs Leech. This position stemmed from Taussig's collaboration with Edward Albert Parks. Parks helped establish the first pediatric speciality clinic at Johns Hopkins Medical School. This interaction was the first step in Taussig's journey into the field of pediatric cardiology. Parks sought for more information in developing a clinic from Dr. Edward Carter. Dr. Carter along with Dr. Benedict Harris and Dr. Helen B. Taussig assisted Dr. Edward Albert Park in the formation of the clinic. Parks' collaboration with the previously mentioned doctors along with the Rockefeller Institute aided in the formation of the first pediatric cardiac disease unit at Johns Hopkins. This was mainly an outpatient dispensary at Johns Hopkins. Parks then formed a second permanent clinic: Harriet Lane Home. Most pediatric clinics at the time focused on rheumatic fever, the major cause of mortality in children at the time. However, due to Taussig's background, in addition to treating for rheumatic fever, Taussig's clinic also specialized in congenital heart deformities.

The Taussig Bing Anomaly was first described in 1949 in which Taussig and Bing encountered a case of a heart with a subpulmonary ventricular septal defect. They described their case as a transposition of the aorta and a levoposition of the pulmonary artery. This anomaly is largely associated with aortic arch obstruction. The anomaly demonstrates the relationship between major arteries and the transposition of the aorta to the right ventricle in which the pulmonary artery slightly abrogates the high ventricular septal defect. Essentially, this defect is known as a double outlet right ventricle in which the great arteries come together either partially or fully from the right ventricle and is characterized by ventricular septal defects. The current surgical treatment for this includes connecting the left ventricle to systemic circulation by a method in which the semilunar valve is connected to the ventricular septal defect.