- ICH GCP
- US Clinical Trials Registry
- Clinical Trial NCT03551600
Splanchnic and Renal Tissue Oxygenation During Enteral Feedings in Neonates With Patent Ductus Arteriosus
Patent ductus arteriosus (PDA) is a common problem in the neonatal intensive care unit and can be secondary to prematurity or congenital heart disease (CHD). PDA is the most common cardiovascular abnormality in preterm infants, and is seen in 55% of infants born at 28 weeks, and 1000 grams or less. In addition to producing heart failure and prolonged respiratory distress or ventilator dependence, PDA has been implicated in development of broncho-pulmonary dysplasia, interventricular hemorrhage, cerebral ischemia, and necrotizing enterocolitis (NEC). In an Israeli population study 5.6% of all very low birth weight infants (VLBW) were diagnosed with NEC, and 9.4% of VLBW infants with PDA were found to have NEC. In a retrospective analysis of neonates with CHD exposed to Prostaglandin E found that the odds of developing NEC increased in infants with single ventricle physiology, especially hypoplastic left heart syndrome. The proposed pathophysiological explanation of NEC and PDA is a result of "diastolic steal" where blood flows in reverse from the mesenteric arteries back into the aorta leading to compromised diastolic blood flow and intestinal hypo-perfusion. Prior studies have demonstrated that infants with a hemodynamically significant PDA have decreased diastolic flow velocity of the mesenteric and renal arteries when measured by Doppler ultrasound, and an attenuated intestinal blood flow response to feedings in the post prandial period compared to infants without PDA. Near Infrared Spectroscopy (NIRS) has also been used to assess regional oxygen saturations (rSO2) in tissues such as the brain, kidney and mesentery in premature infants with PDA. These studies demonstrated lower baseline oxygenation of these tissues in infants with hemodynamically significant PDA. These prior NIRS studies evaluated babies with a median gestational age at the time of study of 10 days or less. It is unknown if this alteration in saturations will persist in extubated neonates with PDA at 12 or more days of life on full enteral feedings.
In the present study the investigators hypothesize that infants with a PDA, whether secondary to prematurity or ductal dependent CHD, will have decreased splanchnic and renal perfusion and rSO2 renal/splanchnic measurements will be decreased during times of increased metabolic demand such as enteral gavage feeding. To test this hypothesis the investigators have designed a prospective observational study utilizing NIRS to record regional saturations at baseline, during feedings, and after feedings for 48 hours.
Study Overview
Status
Conditions
Intervention / Treatment
Study Type
Enrollment (Actual)
Contacts and Locations
Study Contact
- Name: Mariana Baserga, MD
- Phone Number: 801-581-4178
- Email: mariana.baserga@hsc.utah.edu
Study Locations
-
-
Utah
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Murray, Utah, United States, 84107
- Intermountain Medical Center
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Salt Lake City, Utah, United States, 84113
- Primary Children's Hospital
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Salt Lake City, Utah, United States, 84112
- University of Utah Health
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Participation Criteria
Eligibility Criteria
Ages Eligible for Study
Accepts Healthy Volunteers
Genders Eligible for Study
Sampling Method
Study Population
Description
Inclusion Criteria:
PDA secondary to prematurity
- Premature infants of ≤ 32 weeks gestational age at birth
- Patent ductus arteriosus diagnosed via echocardiogram
- Feeding volume ≥ 70 ml/kg/day
- Stable Clinical Condition (no vasopressors, no clinical sepsis)
- Age ≥ 12 days of life
Control group
- Premature infants of ≤ 32 weeks gestational age at birth
- No PDA
- Feeding volume ≥ 70 ml/kg/day
- Stable Clinical Condition (no vasopressors, no clinical sepsis)
- Age ≥ 12 days of life
PDA secondary to CHD and Prostaglandin E (PGE)
- Infants of ≥ 32 weeks gestational age at birth
- Ductal dependant congenital heart disease
- PGE infusion
- No prior cardiac surgery
- Any bolus feedings 10 ml/kg/day or more
- Stable Clinical Condition (no vasopressors, no clinical sepsis)
- Age ≥ 12 days of life
Control Group
- Infants of ≥ 32 weeks gestational age at birth
- No know congenital heart defect including PDA.
- No prior cardiac surgery
- Feeding volume ≥ 1/2 of total fluid volume ~50- 70 ml/kg/day
- Stable Clinical Condition (no vasopressors, no clinical sepsis)
Exclusion Criteria:
- Lack of parental consent
- Multiple congenital anomalies
- Unstable clinical condition
- Prior abdominal pathology (medical/surgical necrotizing enterocolitis within the last 14 days, gastroschisis, or other abdominal abnormality)
Study Plan
How is the study designed?
Design Details
- Observational Models: Cohort
- Time Perspectives: Prospective
Cohorts and Interventions
Group / Cohort |
Intervention / Treatment |
---|---|
Preterm, no PDA
Babies </= 32 weeks gestation at birth with no symptoms of a patent ductus arteriosus (PDA) or echocardiogram confirmation of no PDA Near-infrared spectroscopy (NIRS) monitoring x 48 hours of splanchnic and cranial regions, minimum of 8 feedings need to be recorded |
NIRS analyzes regional oxygen saturations (rSO2)
|
Preterm, moderate to large PDA
Babies </= 32 weeks gestation at birth with confirmed moderate to large PDA on echocardiogram Near-infrared spectroscopy (NIRS) monitoring x 48 hours of splanchnic and cranial regions, minimum of 8 feedings need to be recorded
|
NIRS analyzes regional oxygen saturations (rSO2)
|
>/= 34 wk infants, no CHD
Babies >/= to 34 weeks gestation at birth with no evidence of ductal dependent congenital heart disease (CHD) Near-infrared spectroscopy (NIRS) monitoring x 48 hours of splanchnic, renal and cranial regions, minimum of 8 feedings need to be recorded |
NIRS analyzes regional oxygen saturations (rSO2)
|
>/= 34 week infants, CHD
Babies >/= to 34 weeks gestation at birth with ductal dependent CHD Near-infrared spectroscopy (NIRS) monitoring x 48 hours of splanchnic, renal and cranial regions, minimum of 8 feedings need to be recorded |
NIRS analyzes regional oxygen saturations (rSO2)
|
What is the study measuring?
Primary Outcome Measures
Outcome Measure |
Measure Description |
Time Frame |
---|---|---|
Baseline renal and splanchnic rSO2 measurements
Time Frame: 48 hours
|
Compare the baseline renal and splanchnic rSO2 measurements between preterm, late preterm, and term infants with a patent ductus arteriosus to those infants without a patent ductus arteriosus
|
48 hours
|
Secondary Outcome Measures
Outcome Measure |
Measure Description |
Time Frame |
---|---|---|
Renal and splanchnic rSO2 measurements during feedings
Time Frame: 48 hours
|
Compare the renal and splanchnic rSO2 measurements between preterm, late preterm, and term infants with a patent ductus arteriosus to those infants without a patent ductus arteriosus immediately before, during, and after feedings
|
48 hours
|
Collaborators and Investigators
Sponsor
Collaborators
Study record dates
Study Major Dates
Study Start (Actual)
Primary Completion (Actual)
Study Completion (Actual)
Study Registration Dates
First Submitted
First Submitted That Met QC Criteria
First Posted (Actual)
Study Record Updates
Last Update Posted (Actual)
Last Update Submitted That Met QC Criteria
Last Verified
More Information
Terms related to this study
Additional Relevant MeSH Terms
Other Study ID Numbers
- 83943
Plan for Individual participant data (IPD)
Plan to Share Individual Participant Data (IPD)?
Drug and device information, study documents
Studies a U.S. FDA-regulated drug product
Studies a U.S. FDA-regulated device product
This information was retrieved directly from the website clinicaltrials.gov without any changes. If you have any requests to change, remove or update your study details, please contact register@clinicaltrials.gov. As soon as a change is implemented on clinicaltrials.gov, this will be updated automatically on our website as well.
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