J Perinat Neonat Nurs

CONTINUING EDUCATION Vol. 20, No. 4, pp. 333–340

c 2006 Lippincott Williams & Wilkins, Inc.

Management of the Neonate With Patent

Ductus Arteriosus
Lisa DiMenna, MS, RNC, NNP; Cindy Laabs, MS, RNC, NNP;
Lisa McCoskey, MS, RNC, NNP; Amanda Seals, MS, RNC, NNP

Care of the preterm infant with a suspected or confirmed diagnosis of patent ductus
arteriosus (PDA) is a frequent challenge for the neonatal nurse. Management of term
infants with cardiac lesions dependent upon a PDA can be even more challenging. It is
vital for neonatal nurses to understand the normal cardiovascular and pulmonary
changes that occur at birth so they can anticipate pathological processes influencing
the clinical course of an infant with a PDA. In addition, knowledge of current and
effective treatment approaches is essential to providing optimal care for these
vulnerable infants, as well as in guiding their parents. The purpose of this article is to
review current information about PDA, including physiology, pathophysiology,
pharmacological approaches, surgical considerations, complications and outcomes,
parental support, and areas for future research. Key words: cardiac disease, ibuprofen,
indomethacin, neonates, patent ductus arteriosus

T he ductus arteriosus (DA) is a vital structure in fetal

life that connects the pulmonary artery with the
descending aorta and normally closes with transition
to extrauterine life.1 Failure of the ductus to close after
birth may result in significant clinical problems.2 Patent
ductus arteriosus (PDA) is a common condition in the
premature infant. Although less common, term infants
with congenital heart disease may require patency of
the DA for survival while awaiting correction of their
cardiac defect.
PDA occurs in only approximately 0.02% to 0.006%
of full-term live births.3,4 Premature infants have a
much higher incidence of PDA, up to 45% in neonates
weighing less than 1750 g at birth, and up to 80% of
extremely low birth weight (ELBW) neonates weighing
less than 1000 g.4–6 The incidence of PDA is inversely
related to gestational age and the etiology is thought to
be the result of hypoxia, acidosis, and immature mech-
anisms for ductal closure.1 Perinatal asphyxia, high al-
titude, congenital syndromes (congenital rubella, tri-
somy 13 & 18, and Rubinstein-Taybi), and congenital
heart disease are also associated with higher incidence
of PDA. Antenatal steroids, fetal growth restriction, and
prolonged rupture of membranes prior to delivery are
associated with a lower incidence of PDA, as outlined
in Table 1. Females are affected twice as often as males
when PDA occurs as an isolated event; otherwise, the
distribution between sexes is equal.3
The article describes the physiology and pathophysi-
ology of the DA with emphasis on premature infants. In
addition, clinical manifestations, diagnostic tests, sup-
portive interventions and management goals, compli-
cations, and follow-up of the infant with a PDA are re-
viewed and areas for future research are suggested.
PHYSIOLOGY
Fetal physiology

From the College of Nursing, Arizona State University, Tempe.
Corresponding author: Lisa DiMenna, MS, RNC, NNP, 1335 E June
St, #215, Mesa, AZ 85203 (e-mail: lisannp@cox.net).
Submitted for publication: May 10, 2005
Accepted for publication: May 24, 2005
The DA is a remnant of the distal portion of the left sixth
aortic arch. It connects the main pulmonary artery to
the aorta just below the level of the left subclavian
artery.2,7 During fetal life, the DA is a normal struc-
ture that allows right-to-left diversion of the majority
333
334 Journal of Perinatal & Neonatal Nursing/October–December 2006
Table 1. Factors that affect patent ductus
arteriosus3–6
Factors increasing incidence of patent ductus arteriosus
• Perinatal asphyxia
• High altitude at birth
• Congenital syndromes
Congenital rubella
Trisomy 13 & 18
Rubinstein-Taybi
• Congenital heart disease
• Prematurity
• Sepsis
• Hypoxemia
• Excess IV fluid therapy
Factors decreasing incidence of patent ductus arteriosus
• Maternal steroids
• Fluid restriction
• Increased gestational age
• Intrauterine growth restriction
• Prolonged rupture of membranes
of blood leaving the right ventricle away from the high
resistance and low metabolic needs of the pulmonary
bed to the lower pressure systemic circulation via the
descending aorta (Fig 1). A classic PDA connects at the
junction of the main pulmonary artery and the left pul-
monary artery to the medial aorta below the level of
the left subclavian artery.3 The DA is adequately de-
veloped by 6 weeks’ gestation to carry up to 60% of
the combined ventricular output.2 Ductus arteriosus
patency in utero is thought to be due to the com-
bined effects of a low arterial oxygen tension (PaO2 )
and a high level of circulating prostaglandins, namely,
PGE1 , PGE2 , and prostacyclin (PGI2 ). PGE2 is the ma-
jor factor responsible for relaxation of the smooth
muscle wall of the DA. Prostaglandins are elevated in
the fetus because of the minimal blood flow through
the lungs where prostaglandins are metabolized and
increased production of prostaglandins within the
placenta.2,8
At birth, normal lung oxygenation and ventilation
causes the pulmonary vascular resistance (PVR) to de-
crease, allowing the right ventricular output to enter
the pulmonary circulation. Concurrently, the systemic
vascular resistance (SVR) increases with clamping of
the cord and removal of the low-pressure placenta.2 As
pulmonary blood flow increases, PaO2 rises and PGE2
is metabolized. In response to this rise in PaO2 and de-
crease in circulating prostaglandins, the DA constricts.
The DA remains partially patent in all infants during
early extrauterine adaptation, during which time some
right-to-left blood flow may occur through the ductus
and blood of higher oxygen concentration perfuses the
Figure 1. Pediatric cardiovascular certification course pre-
sented at St. Joseph’s Hospital and Medical Center 1999–
2003 (Author: Suzan Miller-Hoover, MS, RN, CCRN, and
Patricia Hassing, RN, BSN)
ductus.2,6 In preterm infants, ductal closure is often
delayed.
Pathophysiology
Functional closure of the DA occurs usually within the
first 24 to 96 hours of life in a healthy term infant, with
structural obliteration of the DA occurring within 2 to
3 months.1 The process involves necrosis of the inti-
mal (inner) wall of the DA, followed by formation of
fibrous tissue, the ligamentum arteriosum, which per-
manently seals the ductal lumen.2 Delayed closure of
the ductus in the term neonate is due to anatomic de-
fects consisting of an abnormal distribution of elastic
material in ductal tissue and a subendothelial lamina,
which interferes with intimal cushion development.2
Several factors contribute to delayed closure of
the DA in preterm infants. The smooth muscle of
the immature ductus has a diminished response
to oxygen and greater sensitivity to the dilating
action of prostaglandins. Circulating prostaglandins
are also frequently elevated in preterm infants be-
cause of reduced pulmonary metabolism of prostagla-
ndins.2 Surfactant therapy further contributes to the
rapid decrease in PVR, often resulting in a large left-
to-right shunt through the PDA to the pulmonary cir-
culation, especially with earlier gestation infants.5
The preterm myocardium has fewer contractile ele-
ments and more water, with incomplete sympathetic
stimulation of the left ventricle, and low serum cal-
cium levels—common in preterm infants—also affect
myocardial performance. Left ventricular failure may

occur with a PDA because of increased circulation
through the left atrium, left ventricle, and the aorta.
There is overperfusion of the lungs because of elevated
pulmonary blood flow and diastolic pressure, resulting
in a lack of normal postnatal maturational changes of
the small pulmonary arteries.2
ASSESSMENT AND DIAGNOSIS
Classic clinical signs of PDA include a systolic or con-
tinuous machinery murmur loudest at the left upper
sternal border, widening pulse pressures, hypotension,
palmar pulses and/or bounding peripheral pulses, over-
active precordium, and tachycardia.3,4,9 The quality of
the murmur in the premature infant may be rough in
nature. Bounding peripheral pulses are the effect of
high left ventricular stroke volume simulating a systolic
hypertension, followed by a low diastolic pressure due
to overflow into the pulmonary artery from the aorta.
The widened pulse pressure creates a large gradient
and resultant bounding pulse. The drop in diastolic
pressure brings the mean arterial pressure down and
accounts for the systemic hypotension associated with
PDA. This compromised systemic diastolic arterial cir-
culation can result in systemic hypoperfusion, affect-
ing the kidneys and potentially contributing to de-
velopment of volume overload and congestive heart
failure.1,2
Later signs of a symptomatic PDA are tachyp-
nea, tachycardia, apnea, increased precordial activity,
moderate to severe respiratory distress, and cardiac
failure.3,4 Most PDAs result in a left-to-right shunt.
Blood travels the path of least resistance and the higher
systemic pressure drives some of the cardiac output
from the aorta back through the DA into the pulmonary
artery. The blood then recirculates through the lungs in
addition to the normal blood flow from the right ven-
tricle. The additional volume overloads the low pres-
sures of the pulmonary bed and distention of the vas-
cular bed occurs. The primary effect is a ventilation
perfusion mismatch; there is too much blood in the
pulmonary capillaries pushing on the alveoli and im-
pairing gas exchange. These fragile capillaries then be-
come leaky and fluid fills the alveolar sacs, causing the
lung tissue to become thick and less permeable to oxy-
gen and carbon dioxide. If the PDA persists, fluid will
continue to seep and occupy critical space in the avail-
able alveoli for gas exchange to occur. The increased
blood return from the lungs to the left atrium and ulti-
mately left ventricle causes an increased preload. Over
time, the left ventricle will enlarge and lose functional-
ity, resulting in a left-sided heart failure.4
PDA Management in Neonates 335
Diagnostic tests
An echocardiogram (ECHO) is the definitive diagnos-
tic test to evaluate the presence of a PDA and to as-
sess whether or not there is a ductal-dependent le-
sion. An ECHO works by transmitting high frequency
sound waves that bounce off structures and different
tissue densities to form a visual picture of the heart.10
The PDA is best viewed and evaluated through the
suprasternal notch and the parasternal short axis view.
During the ECHO, the diameter of a patent DA can
usually be measured and a color Doppler can show
the direction of blood flow across the PDA. Another
method for assessing the direction of the shunting in a
PDA is comparing preductal and postductal oxygen sat-
urations. The preductal saturation monitor should be
placed on the right hand or wrist and the postductal sat-
uration monitor placed on another extremity, for exam-
ple, the left hand or wrist. Postductal saturations may
be 5% to 10% higher than preductal saturations with
more typical left-to-right shunting. In right-to-left shunt-
ing, preductal saturations will be greater than postduc-
tal saturations (ie, right-hand saturation of 98% versus
left-hand saturation of 93%). Preductal and postductal
saturation differences do not always occur and a differ-
ence in pulse oximeter readings may vary, as affected
by the degree of shunting and whether there is arterial-
venous blood mixing depending on an additional car-
diac malformation such as a patent foramen ovale or
ventricular septal defect. Preductal and postductal sat-
uration readings cannot be considered diagnostic for
PDA; the information should be used only as additional
clinical data if other signs and symptoms of a PDA exist.
Differential diagnoses
Since the signs and symptoms of PDA may initially
be nonspecific, several differential diagnoses must
be considered. Respiratory distress syndrome (RDS)
must be differentiated from other respiratory distress
since most PDAs occur in premature infants who of-
ten also have surfactant deficiency, and respiratory
distress is often one of the first clinical signs of a
functional DA in these neonates. A chest x-ray can
help differentiate RDS versus PDA; lucent or dark air
bronchograms resembling tree branches are indicative
of RDS whereas fluid in the pulmonary vasculature
from the PDA will appear opaque or white. Symp-
tomatic PDA after RDS treatment with surfactant is
common because of the abrupt increase in compli-
ance of the lungs creating a low resistance area for
blood flow unless the infant is on high ventilatory
pressures. Sepsis must also be considered in an in-
fant with respiratory distress, tachycardia, and overall
336 Journal of Perinatal & Neonatal Nursing/October–December 2006
Table 2. Management strategies4
• Prevent hypoxemia and acidosis
• Restrict fluids
• Optimize nutrition
• Maintain central venous hemoglobin 13 g/dL
clinical deterioration. Premature infants are exposed to
numerous people and inanimate objects in the NICU
that along with their immature immune system predis-
pose them to infection. Sepsis must therefore be con-
sidered a serious risk and treatment initiated in the in-
fant who shows signs of PDA and sepsis.
MANAGEMENT
Ongoing management goals
Management goals for the infant at risk for and with
a PDA begin at admission and continue through-
out the hospitalization whether the PDA is closed
with medication or surgically ligated. Initial manage-
ment requires keen assessment of respiratory status.
Standard management goals and strategies include
close clinical monitoring, ventilatory support and fluid
restriction, and insuring adequate/optimal oxygen-
carrying capacity, while facilitating closure of the
PDA (Table 2).4 Following nonsurgical ductal closure,
preventing reopening and clinical decompensation
secondary to increased pulmonary blood flow requires
effective ventilatory support and fluid management
with fluid restriction and cautious fluid adjustments.
Comprehensive clinical management of premature
infants also includes prevention of acidosis, hypoten-
sion, hypoxemia, hypercapnia, intraventricular hemor-
rhage (IVH), and infection. Acidosis, hypotension, and
hypoxemia encourage ductal dilation and premature in-
fants are at greater risk for perinatal stress, hypoxia, and
IVH. Optimizing nutritional status is also an important
focus of care for premature infants.
Supportive interventions and
evaluative goals
Respiratory distress secondary to a PDA often requires
endotracheal intubation and assisted ventilation. In-
creasing positive end-expiratory pressure can reduce
the effects of pulmonary edema. Blood gases for mon-
itoring acidosis, hypoxia, and/or hypercapnia along
with the neonate’s supplemental oxygen requirements
are useful in assessing and managing increased pul-
monary blood flow and reducing the risk of pulmonary
edema. Oxygen-carrying capacity is directly associated
with hemoglobin and hematocrit levels, which must
be monitored closely. Myocardial oxygen delivery de-
pends on blood oxygen content and a low hemoglobin
may increase the potential for ischemia.5 Maintaining
optimal oxygen-carrying capacity improves oxygena-
tion and ventilation, encourages ductal constriction,
and helps insure delivery of oxygen and nutrients to
the systemic tissues and cells, promoting acid-base
balance.5 Fluid restriction can help to minimize the in-
travascular volume that promotes patency of the PDA
and the left-to-right shunting of blood contributing to
accumulation of fluid in the lungs. Infant vital signs and
cardiopulmonary status must be closely monitored to
time and evaluate interventions and assess for any signs
of decompensation. Clinical assessments should focus
on cardiopulmonary functioning, hemodynamic status
including blood pressure and peripheral pulses, venti-
lation and oxygenation, and acid-base balance.
Pharmacologic management
Randomized clinical trials for treatment of PDA in
preterm infants generally fall into 3 categories: prophy-
lactic treatment within 24 hours of birth, treatment fol-
lowing ultrasound evidence of a PDA before symptoms
present or with presentation of the first clinical signs,
and treatment when there is evidence of hemody-
namic changes.11 The optimum timing for intervention
remains controversial. Data pooled from randomized
trials in which prophylactic indomethacin doses were
begun in the first 24 hours after birth have revealed a
reduction in IVH and the need to subsequently treat a
PDA but no changes in mortality, bronchopulmonary
dysplasia (BPD), necrotizing enterocolitis (NEC), or
retinopathy of prematurity (ROP).11
Pharmacological closure of a PDA can be attained
with prostaglandin synthesis inhibitors.12 Of these, in-
domethacin has been used in the treatment of PDA
since 1976.13 This nonsteroidal anti-inflammatory drug
(NSAID) has been effective in treatment, but is as-
sociated with a number of side effects. The use of
indomethacin results in a marked decrease in cere-
bral, mesenteric, and renal blood flow.14 It has also
been associated with electrolyte imbalances, decreased
glomerular filtration rate, and oliguria.15
Intravenous administration of indomethacin in sev-
eral doses or courses has been shown to promote duc-
tal closure in the first 3 to 4 weeks of age, after which
time efficacy diminishes. Other sources describe in-
domethacin as less effective in closing a PDA after
the first 10 to 14 days of life.4,7 Indomethacin can be
given prophylactically, after early signs, or later when

signs persist and compromise the neonate. Often, the
neonate given prophylactic indomethacin has received
surfactant therapy for RDS. A concern regarding pro-
phylactic indomethacin is the lack of evidence that an
infant ever actually had a PDA, potentially resulting in
unnecessary treatment.16
Use of indomethacin upon the neonate’s earliest sign
of a PDA is more common and indomethacin along with
fluid restriction may be the first treatments in manag-
ing a PDA. Contraindications for using indomethacin
include IVH, thrombocytopenia, bleeding other than
pulmonary hemorrhage, NEC, and renal dysfunction.
Neonatal clinical literature also provides information
on the use of intravenous ibuprofen for pharmaco-
logic closure of PDA. Researchers outside of the United
States have examined the use of ibuprofen, another
NSAID and cyclooxygenase blocker, as an alternative
treatment for PDA with fewer side effects compared
with indomethacin.17 A recent trial describes success
in significantly reducing the incidence of PDA in the
preterm infant with a 66% to 80% efficacy rate and with-
out significant adverse effects such as thrombocytope-
nia or compromised urinary output.18 Table 3 presents
general guidelines on indomethacin and ibuprofen ad-
ministration; dosing and frequency vary depending on
hours of age. At least one management handbook states
that clinical studies suggest ibuprofen is as effective as
indomethacin in the treatment of PDA, without reduc-
ing mesenteric and renal blood flow.4
Surgical management
Surgical ligation is the other treatment for PDA. “Most
neonatal units choose indomethacin initially, followed
by surgical closure if the ductus remains patent, al-
though some units with the ready availability of a pe-
diatric cardiothoracic team opt for surgical ligation as
the initial treatment.”11(p69) Surgery is often necessary
when an infant does not respond to pharmacological
treatment and the PDA is symptomatic causing respira-
tory compromise.
Table 3. Pharmacological management of patent ductus arteriosus19–21
Route
Prophylactic indomethacin IV
Short-course indomethacin IV
Long-course indomethacin IV
Ibuprofen IV
PDA Management in Neonates 337
Surgical ligation has a low mortality rate but risks in-
clude hypotension from anesthesia, transient hypoxia
during surgery, infection, postsurgical ventilatory sup-
port due to lung manipulation, the need for pain man-
agement, and additional nutritional needs. The most
common risk of a PDA ligation, as with any surgery,
is infection. This is especially critical because of the
breakdown of the pleural barrier that protects the
heart and lungs. Other potential complications in-
clude bleeding, ligation of the pulmonary artery or
aorta, pneumothoraces, chylothorax, atelectasis, laryn-
geal nerve palsy with paralysis of the vocal cords, and
hypotension. The procedure takes approximately 45
minutes from the time the incision is made to when the
incision is closed. Once the DA is visualized (Fig 2), the
surgeon ties several sutures around the ductus or places
1 to 2 metal clamps across the ductus (Fig 3). Verifi-
cation that the correct blood vessel is clamped is de-
termined by the infant’s continued hemodynamic sta-
bility. Inadvertent clamping of the aorta instead of the
DA would result in a severe drop in the infant’s blood
pressure.
Management of a term infant with PDA is determined
by the clinical severity of symptoms. Cautious fluid re-
striction and diuretics may be sufficient with a small
PDA. Ten percent of all congenital heart disease in term
infants however presents as a PDA.4 The presence of
ductal-dependent lesions must therefore be ruled out
before therapies to close the PDA are initiated. Of-
ten, with the term infant, supportive therapies and
indomethacin are not effective and these infants re-
quire surgical ligation because of impeding pulmonary
congestion.
FOLLOW-UP
Follow-up for closure of a PDA largely depends on
the type of treatment used to close the ductus. If the
PDA is small in size and the infant is asymptomatic,
Length of
Dose/frequency treatment
0.1 mg/kg q24 h 2–3 d
0.2 mg/kg for 1 dose and 0.1 mg/kg for 3d
2 doses q24 h
0.1 mg/kg q24 h 5–7 d
3-dose course: 10 mg/kg 1 dose, 5 mg/kg 3d
2 and 3 dose, q24 h
338 Journal of Perinatal & Neonatal Nursing/October–December 2006

Figure 2. Retrieved from CardioAccess International Clinical Outcomes Database (http://www.cardioaccess.com/pda1.jpg).

Figure 3. Retrieved from CardioAccess International Clinical Outcomes Database (http://www.cardioaccess.com/pda2.jpg).

medical management may include only fluid restriction
and clinical observation. If the infant does well over
several weeks, no further follow-up may be warranted.
A moderate to large PDA is usually treated initially with
indomethacin and followed by an ECHO within 24 to
48 hours after the last dose to evaluate treatment effec-
tiveness. If indomethacin administration fails to close
the PDA (usually multiple courses are attempted), sur-
gical ligation is performed, and follow-up includes mon-
itoring for postsurgical recovery and complications
(Table 4).3,22
POTENTIAL SEQUELAE
Infant outcome following PDA closure is related to the
infant’s preexisting medical condition. Morbidity and
mortality rates have decreased over time for infants
with PDA, yet complications can result, especially if

Table 4. Complications of patent ductus arterio-
sus treatment
Indomethacin
• Decreased urinary output
• Electrolyte imbalances
• Gastrointestinal bleeding/feeding intolerance
• Compromised platelet function and thrombocytopenia
• Potential for mesenteric vasoconstriction
compromising blood flow and resulting
in necrotizing enterocolitis
Surgical ligation
• Hypotension from anesthesia
• Hypoxemia during surgery
• Infection
• Pneumothorax, atelectasis, laryngeal
nerve palsy
• Wound healing complications
pulmonary hypertension or other pulmonary morbid-
ity is involved.3,5 Early ductal closure may improve an
infant’s outcome and alter the clinical course,5 espe-
cially if pulmonary edema and prolonged ventilatory
support can be minimized. The less symptomatic an
infant is prior to closure of the PDA and the more sta-
ble other organ systems are, the more favorable the
prognosis.
Treatment risks exist for medical and surgical PDA
closure. The risk of mortality from surgery is low
and complications including bleeding and risk for
infection are usually minimal.11,22 Fluid restriction
may lead to dehydration and electrolyte imbalance
with potential hypotension due to hypovolemia.23
Indomethacin can result in increased incidence of
NEC, feeding intolerance, oliguria, hypoglycemia,
and thrombocytopenia.24 Extremely premature infants
with significant PDA are at greater risk to develop
BPD because of the need for mechanical ventilatory
support.22 Most infants, however, usually respond well
to PDA management and improve once the ductus is
closed. Posttreatment, the infant usually has enhanced
cardiopulmonary functioning with better hemodynam-
ics, a stable blood pressure and steady pulses, improved
ventilation, oxygenation, and resolving acidosis. Suc-
cessful PDA treatment benefits outweigh the risks and
the significant potential complications associated with
persistent PDA, including congestive heart failure, in-
fective endocarditis, pulmonary vascular obstructive
disease, and aortic rupture.25
PREVENTION
Antenatal use of steroids for premature lung matura-
tion may reduce the incidence of PDA in neonates.16
PDA Management in Neonates 339
Recent studies recommend the use of indomethacin or
ibuprofen prophylactically to prevent a PDA in prema-
ture infants.11,26 However, long-term outcomes remain
unknown for these study groups and additional trials
are recommended to address potential adverse effects
such as pulmonary hypertension and long-term neu-
rodevelopment outcomes.11,18 A Cochrane Review ex-
amined the use of Furosemide for the prevention of
morbidity in indomethacin-treated infants with PDA;
the authors concluded that Furosemide was not a sup-
portive therapy, especially in the presence of dehydra-
tion, and may encourage ductal opening by affecting
prostaglandin metabolism.27 Given that PDA is a pri-
mary problem in premature infants, an indirect way of
preventing the occurrence of PDA is through preven-
tion of premature births.
ANTICIPATORY GUIDANCE/PARENT
EDUCATION
Parental stress in the neonatal intensive care unit is well
known to neonatal nurses and parental support is a
major focus of neonatal nursing care. Any diagnosis or
problem in an infant can be very concerning to parents.
Providing emotional support and educational informa-
tion can help parents gain knowledge and understand-
ing regarding what is going on with their infant. Sup-
plying pictures of the heart showing the PDA may be
an effective visual tool. In addition, providing referrals
and resources can help parents obtain information and
connect with other sources of support (Table 5). Keep-
ing parents informed of their infant’s condition, pro-
viding information regarding what to expect, allowing
them to ask questions and fully participate in the plan
of care, and engaging them in the care of their infant are
essential aspects of anticipatory guidance and partner-
ship building. A multidisciplinary approach facilitates
consistency of information and continuity of care.
Table 5. Resources/Web sites on neonatal patent
ductus arteriosus (PDA) for parents
1. Social services/case management
2. Emily Anderson Center
3. Other parents whose infant had a PDA
4. www.emedicine.com
5. www.pedatrix.com
6. www.nlm.nih.gov (Medline Plus)
7. www.kidshealth.org (Nemours Foundation)
8. www.pediatrics.wisc.edu (For Parents of Preemies)
340 Journal of Perinatal & Neonatal Nursing/October–December 2006
CONCLUSION/IMPLICATIONS FOR FUTURE
RESEARCH
Neonatal nursing care focuses on optimizing care for
fragile premature infants. Neonatal research is impera-
tive in determining the best therapies and practices for
the survival and outcomes. Although PDA is a common
condition in the premature infant population, the tim-
ing and mode of treatments continue to vary. Prompt
and early recognition, as well as anticipation of the
clinical signs of a PDA, are essential in providing ef-
fective treatment and minimizing complications. Fu-
ture research may provide guidelines for care providers
for specific approaches to management. For exam-
ple, antenatal interventions to minimize frequency and
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severity of postnatal PDA may be considered. Random-
ized, experimental control trials may prove beneficial
in comparing other cyclooxygenase inhibitors for the
treatment of PDA closure. Respiratory management ad-
vances and correlation with the incidence and severity
of PDA is another area for further examination. Finally,
comparative study of alternative treatments effectively
utilized in other countries might advance evidence-
based practice. It is important for nurses to stay abreast
of current research and practice literature and utilize
best practices that will positively influence the out-
come of high-risk neonates. Increased knowledge and
understanding of physiology/pathophysiology, phar-
macology, and management of infant conditions will
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