Splanchnic and Renal Tissue Oxygenation During Enteral Feedings in Neonates With Patent Ductus Arteriosus
| Status: | Recruiting |
|---|---|
| Conditions: | Colitis, Peripheral Vascular Disease, Cardiology, Cardiology, Gastrointestinal |
| Therapuetic Areas: | Cardiology / Vascular Diseases, Gastroenterology |
| Healthy: | No |
| Age Range: | Any |
| Updated: | 10/14/2018 |
| Start Date: | October 2015 |
| End Date: | October 30, 2019 |
| Contact: | Katherine Braski, MD |
| Email: | Katherine.Braski@hsc.utah.edu |
| Phone: | 801-213-3915 |
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.
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.
Inclusion Criteria:
- PDA secondary to prematurity
1. Premature infants of ≤ 32 weeks gestational age at birth
2. Patent ductus arteriosus diagnosed via echocardiogram
3. Feeding volume ≥ 70 ml/kg/day
4. Stable Clinical Condition (no vasopressors, no clinical sepsis)
5. Age ≥ 12 days of life
Control group
1. Premature infants of ≤ 32 weeks gestational age at birth
2. No PDA
3. Feeding volume ≥ 70 ml/kg/day
4. Stable Clinical Condition (no vasopressors, no clinical sepsis)
5. Age ≥ 12 days of life
PDA secondary to CHD and Prostaglandin E (PGE)
1. Infants of ≥ 32 weeks gestational age at birth
2. Ductal dependant congenital heart disease
3. PGE infusion
4. No prior cardiac surgery
5. Any bolus feedings 10 ml/kg/day or more
6. Stable Clinical Condition (no vasopressors, no clinical sepsis)
7. Age ≥ 12 days of life
Control Group
1. Infants of ≥ 32 weeks gestational age at birth
2. No know congenital heart defect including PDA.
3. No prior cardiac surgery
4. Feeding volume ≥ 1/2 of total fluid volume ~50- 70 ml/kg/day
5. 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)
We found this trial at
3
sites
5121 S Cottonwood St
Murray, Utah 84157
Murray, Utah 84157
(801) 507-7000
Phone: 801-213-3915
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