Louise Wilkins Haug | Medical Services
Programs & Services
Languages
- English
Louise Wilkins Haug | Education
Undergraduate School
Madison College
1976, Harrisonburg, VA
Graduate School
Medical College of Virginia
1981, Richmond, VA
Medical School
Stanford Medical School
1985, Stanford, CA
Internship
University of Colorado
1986, Denver, CO
Residency
University of Colorado
1989, Denver, CO
Fellowship
Brigham & Women's Hospital
Maternal Fetal Medicine
1992, Boston, MA
Louise Wilkins Haug | Certifications
- American Board of Obstetrics and Gynecology
- American Board of Obstetrics and Gynecology (Maternal and Fetal Medicine)
- American Board of Pediatrics (General)
Louise Wilkins Haug | Professional History
With early career training in human genetics, I saw the unfolding of our understanding of the deep connection between human genetics and pregnancy outcomes – both those pregnancies which proceed without complication and those with unexpected complications such as preterm delivery, preeclampsia or a fetal condition. In these settings, helping a woman and her family navigate the vast information available, prepare for her delivery and develop a support system to sustain her through this process is a challenge and a privilege. My participation with multispecialty care teams provides me daily re-enforcement of their value and the need for patients to be informed as they face a life-changing experience.
As a geneticist, we are only beginning to understand the vast range of genomic contributions to pregnancy outcomes. Continuing to explore how genetics influences a pregnancy is critical. And that what was once considered dogma should always be open for re-analysis. A highlight of my time working in the field of congenital anomalies has been with our fetal cardiac intervention program. Involving a range of specialists, our team showed that the accepted version of a birth defect as a static and predetermined event may not always be true. Some birth defects may result from progressive change through a pregnancy. For a subgroup of fetuses with hypoplastic left heart syndrome, we demonstrated that stenosis of the aortic valve can be the primary event. As the pregnancy continues progressive loss of fetal left ventricle function occurs and results in a newborn with classic HLHS. Most importantly, “in utero” valve dilation of the aortic valve stenosis can prevent further damage to the left ventricle. Over the past 15 years, this team has worked on perfecting and minimizing maternal risks of the procedure, identifying key imaging criteria, and explored at the biologic level how to differentiate the degree of fetal heart damage. As the primary fetal interventionist for this team since 2000, the progress made in both the technique and the outcomes for these children has been a gift.