Splanchnic and Renal Tissue Oxygenation During Enteral Feedings in Neonates With Patent Ductus Arteriosus

Sponsor

University of Utah (Other)

Overall Status

Recruiting

CT.gov ID

NCT03551600

Collaborator

Intermountain Health Care, Inc. (Other)

Enrollment

Locations

Anticipated Duration (Months)

23.3

Patients Per Site

0.3

Patients Per Site Per Month

Study Details

Study Description

Brief Summary

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.

Condition or Disease	Intervention/Treatment	Phase
Infant, Premature Congenital Heart Disease Patent Ductus Arteriosus Necrotizing Enterocolitis	Procedure: Near-infrared spectroscopy (NIRS)

Study Design

Study Type:

Observational

Anticipated Enrollment :

70 participants

Observational Model:

Cohort

Time Perspective:

Prospective

Official Title:

Splanchnic and Renal Tissue Oxygenation During Enteral Feedings in Neonates With Patent Ductus Arteriosus

Actual Study Start Date :

Oct 1, 2015

Anticipated Primary Completion Date :

Jun 30, 2022

Anticipated Study Completion Date :

Jun 30, 2022

Arms and Interventions

Arm	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	Procedure: Near-infrared spectroscopy (NIRS) 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	Procedure: Near-infrared spectroscopy (NIRS) 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	Procedure: Near-infrared spectroscopy (NIRS) 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	Procedure: Near-infrared spectroscopy (NIRS) NIRS analyzes regional oxygen saturations (rSO2)

Outcome Measures

Primary Outcome Measures

Baseline renal and splanchnic rSO2 measurements [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

Secondary Outcome Measures

Renal and splanchnic rSO2 measurements during feedings [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

Eligibility Criteria

Criteria

Ages Eligible for Study:

12 Days to 6 Months

Sexes Eligible for Study:

All

Accepts Healthy Volunteers:

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)

Contacts and Locations

Locations

	Site	City	State	Country	Postal Code
1	Intermountain Medical Center	Murray	Utah	United States	84107
2	University of Utah Health	Salt Lake City	Utah	United States	84112
3	Primary Children's Hospital	Salt Lake City	Utah	United States	84113