1. Duke Fetal Bonding Program
Dr. Jay Campbell, Dr. Piers Barker, and Madden Brewster
DukePediatric Cardiology, DukeUniversity Medical Center

2. Abstract:
The object of the following clinical study is to evaluate the success of the
Duke Cardiology Fetal Bonding Protocol in standard risk CHD patients as well as
examine APGAR scores and weights of patients who did and did not have successful
bonding and finally, to discuss the maternal and infant benefits of the program.
Chart review and statistical analysis of a population of 98 patients was used to
determine a 62% (n=49) successful bonding rate in those who planned bonding
(n=79). Additionally, those where successful bonding did not successfully occur,
lower APGAR scores and birth weights were presented. Mother-infant bonding is
said to promote strong and lasting emotional ties, between mother and child,
provide physiological stability and autonomic maturity, benefit infant emotional
complexes, and allow for breastfeeding if the mother chooses to do so. Overall, the
study provides a comprehensive look at the success as well as the maternal and
infant benefits of the Duke Fetal Bonding Program.
Background and Significance:
Echocardiography (cardiac echo) is a technology that uses Doppler
ultrasound (sound waves) to create two and three-dimensional images of the heart.
Echocardiography is especially useful in determining congenital heart disease (CHD)
in fetuses with a high level of accuracy. (Connolly and Oh, 2011). Currently, many
hospitals use fetal cardiac echo technology to determine CHD in babies prior to birth
to determine where the infant will be transferred to directly after birth (i.e.

3. operating room, pediatric cardiac intensive care unit (PCICU), neonatal intensive
care unit (NICU), or nursery care) (“Congenital heart disease and defects,” n.d.). The
removal of infants from mothers directly after birth causes forfeiture of invaluable
mother-infant bonding time.
Many studies have indicated that mother-infant bonding is important in
developing strong emotional ties between mother and child (O’Higgins et al., 2013).
Additionally, the already stressful process of pregnancy is bombarded with more
undue stress when the mother of a child with CHD is told that she will not get to
engage in the typical mother-infant bonding period because her baby will be
transferred to the PCICU, NICU, nursery care, or even the operating room directly
after birth. This excessive prenatal stress has been linked to have effects on infant
neurodevelopment. (Schneider et al., 1999, Coe et al., 2001, and Chapillon et al.,
2001).
In another 2012 study by Moore et al. early skin-to-skin contact (SSC) during
initial bonding periods is discussed and suggests that it may play an important role
in physiological and emotional complexes in the infant by benefiting breastfeeding
habits, cardio-respiratory stability, and a reducing infant crying. During initial
bonding, the mother is encouraged to breastfeed her newborn. This initial and later
continuation of maternal breastfeeding time has been shown to produce a higher
quality relationship between mother and child at 1 year compared to non-maternal
bottle-feeding groups (Else-Quest et al, 2003).
A recent 2014 study by Feldman et al. showed that preterm infants, who
engage in Kangaroo Care (KC) intervention, where mother and infant maintain close

4. skin to skin contact, showed better autonomic functioning, sleep efficiency, and
executive function. Prior studies suggest that KC intervention also encourages
neuromaturation. (Feldman et al., 2014).
Duke Pediatric Cardiology and OB/GYN departments, have joined together to
create the Fetal Bonding Program at Duke, which allows mother-infant bonding time
and consequently permits potential emotional and physical benefits to both mother
and child.
Literature suggests that the ductus arteriosus (figure 1) in babies does not
close until 12-24 hours after birth on average (Lim et al., 1992 and Reller et al.,
1988). Many congenital heart diseases, like hypoplastic left heart syndrome for
example, do not present themselves and/or cause life-threatening complications
until after the closure of the ductus arteriosus. The ductus arteriosus is a canal,
which connects the pulmonary artery to the descending aorta so that the already
oxygen-rich blood from the placenta can bypass the fluid filled lungs and be
distributed directly to the body. Often times, 12 hours after birth, before the ductus
closes, all babies will experience the pumping of some “blue blood” (deoxygenated
blood), which escapes through the still open ductus, to the body in coalescence with
the “red blood” (oxygenated blood), which passes through the lungs and out of the
aorta. Once the ductus closes, healthy babies will see the distribution of oxygen rich
blood only, because blue blood can no longer escape through the now closed ductus.
(“Congenital heart disease and defects,” n.d.).

5. Figure1: Shows the ductus arteriosis and basic fetal circulation. Source: https://encrypted-
tbn0.gstatic.com/images?q=tbn:ANd9GcTe314OzsM_3sH5-CZg6t3soAj0VE_HxxOpdyVYyqz9w1O8oPlV
There are both right and left sided obstructive congenital heart disease,
which rely on the presence of the ductus arteriosis for survival. For example, a
common left sided obstructive heart disease, hypoplastic left heart syndrome
(HLHS), displays a small aorta and left ventricle/atrium. Because of this, the minimal
amount of red blood that passes through the aorta will primarily go towards the
head. The blue blood from the pulmonary artery will be able to connect to the
descending aorta to distribute blood to the lower body through the ductus. While
this blood is not well oxygenated, it allows for short-term function. This, however,
can become life threatening as the ductus arteriosis closes because there will no
longer be that connection between the pulmonary artery and the descending aorta
and therefore there will be little to no blood flow down to the lower body. HLHS will
present major problems after the ductus closes. (See figure 2). (“Facts about HLHS,”
2012)

6. Figure2: This is an example of the anatomy of hypoplastic left heart syndrome(HLHS) versus a normal
heart. As you can see in the HLHS heart, the left sideof the heart as well as the aorta is very small. The
HLHS figurealso contains a “patent ductus arteriosis” which is what allows infants to survive beforeit
closes. Source:
http://umm.edu/~/media/UMM/Images/Centers%20and%20Services/Childrens%20Hospital/hypopla
stic%20left%20heart%20synd.ashx
Another example of when the presence of the ductus arteriosis allows for
short-term survival is in pulmonary atresia, which is a right-sided obstructive heart
disease. In pulmonary atresia, the pulmonary valve is not formed and therefore
deoxygenated blood is unable to go to the lungs to gain oxygen. The ductus
arteriosis as well as the atrial septal defect (hole in the atrial wall of the heart that
separates the left and right atrium) that all fetuses have in order for blood to bypass
the lungs and go directly to the left ventricle is important for blood flow the body in
a patient with pulmonary atresia. The ductus allows blue blood to enter the aorta,
but go back to the pulmonary artery to gain oxygen before returning to the left

7. ventricle to be pumped out to the body. The blood that goes to the body is “mixed”
(a mixture of red and blue—oxygenated and deoxygenated blood), but allows for
short-term function. Once the ductus arteriosis closes, pulmonary atresia becomes
fatal if it is not corrected because all blood going to the body will be deoxygenated.
(See figure 3). (“Pulmonary Atresia,” n.d.)
Figure3: This is a diagram which shows the anatomy of pulmonary atresia in a fetus/new born who still
has the ductus arteriosis. Source: http://www.heart.org/idc/groups/heart-
public/@wcm/@private/@hcm/documents/image/ucm_307329@z_extracted~1/medium.jpg
With the use of echocardiograph technology we can predict many congenital
heart diseases prior to birth. Additionally, with the presence of the ductus arteriosis
for 12-24 hours after birth, many of these CHD’s don’t present themselves until after
that period. Because of this, we are able to allow valuable mother-infant bonding

8. time, thus reducing prenatal stress, potential neurodevelopment and behavioral
issues, and other negative outcomes that are suggested affects caused by lack of
bonding.
Methods:
Patient charts were reviewed to gather data for this clinical study.
Information such as triage number, “was bonding planned?,” “did bonding actually
occur?,” APGAR scores, and infant birth weights were recorded in an excel
spreadsheet. Statistics software was used to complete univariate comparisons and
statistical analysis of the data.

9. Figure4: This is the protocol followed bythe Duke Fetal Bonding Program to determine whether CHDinfants are healthy enough
to be allotted mother-infant bonding time. Source: Duke Hospital

10. Results:
The sample consisted of 135 mothers and their prenatally diagnosed CHD
infants who qualified for and wished to participate in the Duke Fetal Bonding
Program. Of those, 37 were excluded due to termination of pregnancy (n=4), fetal
demise (n=2), or a delivery that occurred outside of Duke at another hospital
(n=31). Each subject within the remaining population (n=98) had a delivery plan
based on triage status. A triage status above a 2 did not plan bonding after the
delivery (n=19). When bonding wasn’t planned due to a high triage status, it
typically indicated a severe CHD, high risk for mother and/or baby, or other non-
cardiovascular related issues. Those where bonding was planned (n=79) continued
to follow the Heart for Bonding Initiative protocol (see figure 4). While bonding was
planned for many, it may not have been carried out for a variety of usually common,
unexpected birthing complications (n=30). The subjects who completed bonding
successfully (planned, occurred, and without complication) had a population of 49.
This gave a successful bonding rate of 62% in the population. (See Figure 5).

11. Figure5: Displays breakdown of data analysis to determine bonding success inthe Duke Fetal Bonding
Program.
APGAR scores and birth weights were analyzed in both successful bonding
and unsuccessful bonding populations. As shown in figure 6, the mean birth weight
for those who did not have successful bonding (no) is lower (weight=2.62kg) than
those who did have successful bonding (yes) (weight=3.25kg). This result is
Fetal Bonding
Program
population
(n=135)
Excluded (n=37;
27%):
Termination
(n=4)
Fetal Demise
(n=2)
Not delivered at
Duke (n=31)
Fetal Bonding
Program population
with exclusions
(n=98; 73%)
Bonding Planned
(n=79; 80%)
Bonding
Occurred (n=49;
62%)

12. statistically significant (p=0.0026).
Figure6: The above box and whiskers plotdisplays mean infant weights in those who had successful
bonding (Yes) and those who did not (No). (p=0.0026).
APGAR (see figure 7) scores at 1 minute and 5 minutes were also examined
in successful and unsuccessful bonding populations. Figure 8 displays APGAR scores
at 1 minute. It is evident that scores are higher in a majority of those who had
successful bonding (89.80% in 7-10 range) whereas the APGAR scores in those who
did not have successful bonding had a spread out range of scores. This analysis was
statistically significant (p=0.000).

13. Figure7: Apgar scoringsystem for newborn infants. Source:
http://r2.cygnuspub.com/files/cygnus/image/EMSR/2012/JAN/600x400/apgar_10616033.jpg
Figure8: This table displays the frequency and percentage of those who had 1-minute APGAR scores
within ranges 0-3, 4-6, and 7-10 in populations who did (yes) and did not (no) have successful bonding.
(p=0.000).

14. APGAR scores at 5 minutes were a slightly more similar between successful
and unsuccessful bonding groups. Figure 9 shows both successful (yes) and
unsuccessful (no) bonding groups had a majority in the 7-10 range at 5 minutes,
however, all but one in the successful bonding group were in the 7-10 range
whereas the unsuccessful bonding group was a little bit more spread out. This is
statistically significant (p=0.011).
Figure9: This table displays the frequency and percentage of those who had 5-minute APGAR scores
within ranges 0-3, 4-6, and 7-10 in populations who did (yes) and did not (no) have successful bonding.
(p=0.011).
Discussion:
Statistical analysis supports our hypothesis that bonding can be completed
successfully in a majority of standard risk CHD patients. While 62% seems like a
rather low percentage for those to successfully complete bonding, it is a huge
improvement from typical prenatally diagnosed CHD patient success rate. Because
most hospitals do not allow mother-infant bonding in CHD patients, our program
essentially allows for the transition from a 0% to 62% successful bonding rate.
Improving emotional and physiological complexes, mother-infant long-term
relationship, and breastfeeding ability are potential benefits that may occur in those
who successfully completed bonding in the Duke Fetal Bonding Program (O’Higgins

15. et al., 2013, Else-Quest et al, 2003, Feldman et al., 2014). Additionally, the success
rate of bonding in our study may ensure mothers that they will be able to bond with
their prenatally diagnosed CHD babies and reduce the hazardous prenatal stress
presented at initial diagnosis (Schneider et al., 1999, Coe et al., 2001, and Chapillon
et al., 2001).
Our hypothesis that those who did not have successful bonding would
present lower APGAR scored and birth weights was supported. This result was
intuitive and expected. APGAR scores are given at 1 and 5 minutes to determine the
health of the baby and if intervention is needed. Babies with dangerously low or
borderline dangerously low scores were most likely flagged by the caregiver and
transported elsewhere to be taken care of—ultimately forgoing initial mother-infant
bonding time. Non-cardiovascular problems or cardiovascular issues that weren’t
prenatally diagnosed would also contribute to lower APGAR scores and
consequently would not be allowed to bond in some cases. (“What Is The Apgar
Score?” n.d.)
Average birth weights in infants were lower in those who did not have
successful bonding, which also supported our hypothesis. The average birth weight
for a healthy baby is about 3.4 kg and while those who successfully bonded had an
average birth weight lower than that (3.25 kg), those who unsuccessfully bonded
had a birth weight far below the normal average (2.62 kg) (“Infant,” 2014). This low
birth weight most likely contributed to lower APGAR scores and decreased
autonomic function, which ultimately reduced the likelihood of successful bonding.
Additionally, premature babies tend to have lower birth weights and additional

16. health risks which may also explain why those who did not bond successfully had
lower birth rates, however additional analysis involving gestational age would have
to be assessed to support this notion (“A Primer on Preemies,” 2014).
This specific study provides a platform for safe methods and protocols to
allow successful bonding in standard risk congenital heart disease patients. Some
things worth further examining in this study is gestational age between the two
groups as well as diagnosis patterns. Gestational ages may allows us to predict the
likelihood of premature babies to bond. Diagnosis patterns will also allow us to
prenatally predict the likelihood of bonding in those with certain CHD. Finally, the
ultimate goal of this study was to prove that is has no adverse affects and encourage
other hospitals to adopt similar programs.
Conclusion:
Through the safety of the Duke Mother-infant Bonding Program as well as
the benefits of mother-infant bonding and possible reduction of prenatal stress we
hope to encourage other hospitals to use echocardiograph technology to prenatally
diagnose CHD so that a similar protocol to the Duke Fetal Bonding Program is
implemented so that infants with CHD are able to bond with their mothers directly
after birth and do not develop potential deficits due to lack of bonding. Overall, we
would like to see more babies born with CHD able to engage in mother-infant
bonding so that neurodevelopmental and emotional issues do not ensue.

17. References:
"A Primer on Preemies." KidsHealth. Ed. Elana Pearl Ben-Joseph. The Nemours
Foundation, 01 Jan. 2014. Web. 20 May 2014.
<http://kidshealth.org/parent/growth/growing/preemies.html>.
Chapillon P, Patin V, Roy V, Vincent A, Caston J. (2001). Effects or pre- and postnatal
stimulation on developmental, emotional, and cognitive aspects in rodents: A
review. Wiley Periodicals. 373-387.
Coe CL, Lulback GR, Schneider ML. (2001). Prenatal disturbance alters the size of the
corpus callosum in young monkeys. Developmental Psychobiology. 41: 178-
185.
“Congenital Heart Disease and Defects.” Children's Hospital of Wisconsin. Children's
Hospital in Wisconsin, n.d. Web. 12 Jan. 2014.
Connolly HM, Oh JK. Echocardiography. In: Bonow RO, Mann DL, Zipes DP, Libby P,
eds. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 9th
ed. Philadelphia, Pa: Saunders Elsevier;2011: chap 15.
Else-Quest NM, Hyde JS, Clark R. (2003). Breastfeeding, Bonding, and the Mother-
Infant Relationship. Merrill Palmer Quarterly. 49(4): 495-517.
"Facts about Hypoplastic Left Heart Syndrome." Centers for Disease Control and
Prevention. Centers for Disease Control and Prevention, 28 Mar. 2013. Web.
21 Jan. 2014.
"Fact Sheets." The Children's Heart Foundation. N.p., 2012. Web. 09 Jan. 2014.
"Infant." Wikipedia. Wikimedia Foundation, 12 May 2014. Web. 20 May 2014.
<http://en.wikipedia.org/wiki/Infant>.

18. Lim MK, Hanretty K, Houston AB, Lilley S, Murtagh EP. (1992). Intermittent ductal
patency in healthy newborn infants: demonstration by colour Doppler flow
mapping. Archives of Disease in Childhood. 67: 1217-1218.
Moore ER, Anderson GC, Bergman M, Dowswell T. (2012). Early skin-to-skin contact
for mothers and their healthy newborn infants. Cochrane Database System
Review. (3).
"Pulmonary Atresia (PA)." LCPH. Lucille Packard's Children's Hospital at Stanford,
n.d. Web. 21 Jan. 2014.
Ray JG, Urquia ML, Berger H, Vermeulen MJ. (2012). Maternal and neonatal
separation and mortality associated with concurrent admissions to intensive
care units. CMAJ. 184(18): 956-962.
Reller MD, Ziegler ML, Rice MJ, Solin RC, McDonald RW. (1988). Duration of ductal
shunting in healthy preterm infants: an echocardiographic color flow
Doppler study. J Pediatr. 112(3):441-446.
Schneider ML, Roughton EC, Koehler AJ, Lubach GR. (1999). Growth and
development following prenatal stress exposure in primates: An examination
of ontogenetic vulnerability. Child Development. 70(2): 263-273.
“What Is the Apgar Score?” KidsHealth. N.p., n.d. Web. 12 Jan. 2014.