Transcutaneous Carbon Dioxide Monitoring in Neonates Receiving Therapeutic Hypothermia for Neonatal Encephalopathy
NCT ID: NCT04603547
Last Updated: 2025-08-21
Study Results
Results pending
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
Get a concise snapshot of the trial, including recruitment status, study phase, enrollment targets, and key timeline milestones.
Recruitment Status
ACTIVE_NOT_RECRUITING
Total Enrollment
53 participants
Study Classification
OBSERVATIONAL
Study Start Date
2019-09-28
Study Completion Date
2025-10-30
Brief Summary
Review the sponsor-provided synopsis that highlights what the study is about and why it is being conducted.
The aim of our study is to evaluate the feasibility of applying transcutaneous CO2 monitoring (tcPCO2) in neonates receiving therapeutic hypothermia and to quantify the agreement between tcPCO2 and PCO2 in this population with or without respiratory support. Although, transcutaneous measurement of CO2 tension is the most commonly used non-invasive CO2 monitoring system in neonatal intensive care, to date tcPCO2 technique has not been evaluated systematically or used routinely in the intensive care of infants with neonatal encephalopathy receiving hypothermia treatment.
Related Clinical Trials
Explore similar clinical trials based on study characteristics and research focus.
Preemie Hypothermia for Neonatal Encephalopathy
NCT01793129
Infant, Newborn
Hypoxia, Brain
Hypoxia-Ischemia, Brain
+3 more
COMPLETED
NA
Hypoxic-Ischemic Encephalopathy Therapy Optimization in Neonates for Better Neuroprotection With Inhalative CO2
NCT02700854
Hypoxic-Ischaemic Encephalopathy
Perinatal Asphyxia
Hypocapnia
COMPLETED
PHASE1
Whole-Body Cooling for Birth Asphyxia in Term Infants
NCT00005772
Infant, Newborn
Hypoxia-Ischemia, Brain
COMPLETED
PHASE3
Late Hypothermia for Hypoxic-Ischemic Encephalopathy
NCT00614744
Infant, Newborn
Hypoxia, Brain
Hypoxia-Ischemia, Brain
+3 more
COMPLETED
NA
Co2 Monitoring at Preterm Delivery-Observational Study
NCT04699708
Resuscitation
UNKNOWN
Detailed Description
Dive into the extended narrative that explains the scientific background, objectives, and procedures in greater depth.
Neonatal encephalopathy (NE) affects 3 infants per 1000 live birth every year and can lead to death or permanent neurological deficit. Therapeutic hypothermia (33.5 oC) (TH) has been clearly proven to reduce mortality and adverse neurodevelopmental outcome in patients with moderate to severe NE. However, even with hypothermia, nearly half of the infants with NE are at risk of death or severe disability. Optimization of intensive care of these neonates might have the potential to prevent injury progression and further improve neurodevelopmental outcomes.
Multiple analyses noted a high rate (6 -89%) of incidence of hypocarbia during the first hours of postnatal life possibly due to the strong respiratory effort secondary to metabolic acidosis and the hypothermia treatment which causes a 20-30% reduction in metabolic rate. Furthermore, several studies have shown the association between hypocarbia and the increased risk of adverse neurodevelopmental outcome in infants with NE. Hypocarbia has the potential to exacerbate brain injury via multiple mechanisms. Hypocarbia was associated with nuclear DNA fragmentation in the cerebral cortex, membrane lipid peroxidation and increased neuronal excitability in animal models.
It is well established, that carbon dioxide is one of the most potent regulator of cerebral blood flow (CBF), with hypercarbia causing cerebral vasodilation and increased cerebral blood flow by 1 to 2 ml/100g/minute per 1 mmHg in PaCO2, whereas hypocarbia causes cerebral vasoconstriction. Reducing PaCO2 to 20 to 25 mmHg decreases CBF by 40 to 50%.
Hypocarbia may decrease oxygen supply further due to the cerebral vasoconstriction and the leftward shift of oxyhemoglobin curve.
It has been well known for decades that hypocarbia is associated with periventricular leukomalacia and, or, cerebral palsy in preterm neonates. In term, asphyxiated neonates the secondary analysis of the landmark CoolCap and NICHD hypothermia trials established that hypocarbia has a dose-dependent effect on long term neurodevelopmental outcomes. Both minimum and cumulative exposure to PCO2 less than 35 mmHg within the first 12 hours of life increased the risk of death and adverse neurodevelopmental outcome in the secondary analysis of NICHD trial. Consistent with this, the post-hoc analysis of CoolCap study showed that the probability of unfavorable outcome was raised dose-dependently with decreasing PCO2 in infants with moderate and severe NE. Moreover, a recent retrospective study also reported an association between hypocarbia over the first 4 days of life and brain injury on MRI. The consistent findings of an association between hypocarbia and adverse outcomes suggest that the close monitoring of carbon dioxide exchange and the avoidance of hypocarbia is highly important in this vulnerable patient population.
Arterial blood gas analysis, the gold standard for monitoring the respiratory components of acid-base homeostasis, has obvious limitations that preclude its continuous use to follow the dynamically changing level of PCO2. Moreover, repeated arterial samplings can lead to significant blood loss and an increased risk of bacteremia.
Alternative, non-invasive monitoring techniques have been developed to measure PCO2 trends continuously. Transcutaneous measurement of CO2 tension is the most commonly used non-invasive CO2 monitoring system in neonatal intensive care and several studies demonstrated a good agreement between the PCO2 in blood samples and tcPCO2 in premature infants.
In clinical settings, the tcPCO2 measurement is influenced by many factors and is rather to be used as a trend than an absolute number. Clinical conditions such as hypoperfusion due to shock or acidosis, edema of the subcutaneous tissues, vasoconstriction due to vasoactive agents or lower body temperature may alter the tcPCO2 measurement.
Over and underestimates may occur in the extreme high and low range of tcPCO2 measurements.
The sensor of the device heated up to a constant temperature leading to hyperperfusion of the capillaries and increase of the metabolic rate of the skin by approximately 4-5% per every degree Celsius and consequently the gas solubility and diffusion improves. The sensor calculates the PCO2 electrochemically, by change in pH of an electrolyte solution. After a temperature correction to 37 oC the device provides an estimate of skin surface CO2. Higher temperature of the sensor might be associated with better correlation but also might increase the risk of thermal injury.
In addition, tcPCO2 is recommended to all patients undergoing therapeutic hypothermia if the patient receives respiratory support. In the present study our aim is to measure PCO2 continuously in infants undergoing TH with or without respiratory support in order to evaluate its feasibility in cooled infants.
As detailed above, changes in pCO2 affect cerebral perfusion. Therefore, it is important to analyze the cerebral oxygenation and metabolism with the association of PCO2 trends. Continuous cerebral regional oxygen saturation (CrSO2) monitoring has been already used routinely in the intensive care of the infants with NE by using Near Infrared Spectroscopy (NIRS). NIRS is a non-invasive tool that can be used to measure changes in oxygenated, deoxygenated, and total hemoglobin of brain tissue from which cerebral regional oxygen saturation can be derived as a surrogate of cerebral oxygen consumption. A significant positive correlation was found between transcutaneous PCO2 levels and tissue oxygenation index in preterm infants. In line with this, an acute increase in end tidal CO2 (etCO2) was associated with an increase in cerebral oxygenation, whereas an acute decrease was associated with reduced cerebral oxygenation. The tcPCO2 and etCO2 were used as a surrogate marker of PCO2.
Although continuous CO2 monitoring would be desirable in this patient population, to date tcPCO2 technique has not been evaluated systematically or used routinely in the intensive care of infants with neonatal encephalopathy receiving TH. Continuous monitoring may allow to avoid the extreme levels and the fluctuation of PCO2 and may improve the intensive care and the long-term outcomes of infants with NE. The monitoring of cerebral oxygenation by using NIRS together with tcPCO2 measurements can be beneficial for infants with NE and can help to understand the pathophysiology of autoregulation in this specific patient population.
Multiple analyses noted a high rate (6 -89%) of incidence of hypocarbia during the first hours of postnatal life possibly due to the strong respiratory effort secondary to metabolic acidosis and the hypothermia treatment which causes a 20-30% reduction in metabolic rate. Furthermore, several studies have shown the association between hypocarbia and the increased risk of adverse neurodevelopmental outcome in infants with NE. Hypocarbia has the potential to exacerbate brain injury via multiple mechanisms. Hypocarbia was associated with nuclear DNA fragmentation in the cerebral cortex, membrane lipid peroxidation and increased neuronal excitability in animal models.
It is well established, that carbon dioxide is one of the most potent regulator of cerebral blood flow (CBF), with hypercarbia causing cerebral vasodilation and increased cerebral blood flow by 1 to 2 ml/100g/minute per 1 mmHg in PaCO2, whereas hypocarbia causes cerebral vasoconstriction. Reducing PaCO2 to 20 to 25 mmHg decreases CBF by 40 to 50%.
Hypocarbia may decrease oxygen supply further due to the cerebral vasoconstriction and the leftward shift of oxyhemoglobin curve.
It has been well known for decades that hypocarbia is associated with periventricular leukomalacia and, or, cerebral palsy in preterm neonates. In term, asphyxiated neonates the secondary analysis of the landmark CoolCap and NICHD hypothermia trials established that hypocarbia has a dose-dependent effect on long term neurodevelopmental outcomes. Both minimum and cumulative exposure to PCO2 less than 35 mmHg within the first 12 hours of life increased the risk of death and adverse neurodevelopmental outcome in the secondary analysis of NICHD trial. Consistent with this, the post-hoc analysis of CoolCap study showed that the probability of unfavorable outcome was raised dose-dependently with decreasing PCO2 in infants with moderate and severe NE. Moreover, a recent retrospective study also reported an association between hypocarbia over the first 4 days of life and brain injury on MRI. The consistent findings of an association between hypocarbia and adverse outcomes suggest that the close monitoring of carbon dioxide exchange and the avoidance of hypocarbia is highly important in this vulnerable patient population.
Arterial blood gas analysis, the gold standard for monitoring the respiratory components of acid-base homeostasis, has obvious limitations that preclude its continuous use to follow the dynamically changing level of PCO2. Moreover, repeated arterial samplings can lead to significant blood loss and an increased risk of bacteremia.
Alternative, non-invasive monitoring techniques have been developed to measure PCO2 trends continuously. Transcutaneous measurement of CO2 tension is the most commonly used non-invasive CO2 monitoring system in neonatal intensive care and several studies demonstrated a good agreement between the PCO2 in blood samples and tcPCO2 in premature infants.
In clinical settings, the tcPCO2 measurement is influenced by many factors and is rather to be used as a trend than an absolute number. Clinical conditions such as hypoperfusion due to shock or acidosis, edema of the subcutaneous tissues, vasoconstriction due to vasoactive agents or lower body temperature may alter the tcPCO2 measurement.
Over and underestimates may occur in the extreme high and low range of tcPCO2 measurements.
The sensor of the device heated up to a constant temperature leading to hyperperfusion of the capillaries and increase of the metabolic rate of the skin by approximately 4-5% per every degree Celsius and consequently the gas solubility and diffusion improves. The sensor calculates the PCO2 electrochemically, by change in pH of an electrolyte solution. After a temperature correction to 37 oC the device provides an estimate of skin surface CO2. Higher temperature of the sensor might be associated with better correlation but also might increase the risk of thermal injury.
In addition, tcPCO2 is recommended to all patients undergoing therapeutic hypothermia if the patient receives respiratory support. In the present study our aim is to measure PCO2 continuously in infants undergoing TH with or without respiratory support in order to evaluate its feasibility in cooled infants.
As detailed above, changes in pCO2 affect cerebral perfusion. Therefore, it is important to analyze the cerebral oxygenation and metabolism with the association of PCO2 trends. Continuous cerebral regional oxygen saturation (CrSO2) monitoring has been already used routinely in the intensive care of the infants with NE by using Near Infrared Spectroscopy (NIRS). NIRS is a non-invasive tool that can be used to measure changes in oxygenated, deoxygenated, and total hemoglobin of brain tissue from which cerebral regional oxygen saturation can be derived as a surrogate of cerebral oxygen consumption. A significant positive correlation was found between transcutaneous PCO2 levels and tissue oxygenation index in preterm infants. In line with this, an acute increase in end tidal CO2 (etCO2) was associated with an increase in cerebral oxygenation, whereas an acute decrease was associated with reduced cerebral oxygenation. The tcPCO2 and etCO2 were used as a surrogate marker of PCO2.
Although continuous CO2 monitoring would be desirable in this patient population, to date tcPCO2 technique has not been evaluated systematically or used routinely in the intensive care of infants with neonatal encephalopathy receiving TH. Continuous monitoring may allow to avoid the extreme levels and the fluctuation of PCO2 and may improve the intensive care and the long-term outcomes of infants with NE. The monitoring of cerebral oxygenation by using NIRS together with tcPCO2 measurements can be beneficial for infants with NE and can help to understand the pathophysiology of autoregulation in this specific patient population.
Conditions
See the medical conditions and disease areas that this research is targeting or investigating.
Neonatal Encephalopathy
Study Design
Understand how the trial is structured, including allocation methods, masking strategies, primary purpose, and other design elements.
Observational Model Type
COHORT
Study Time Perspective
PROSPECTIVE
Interventions
Learn about the drugs, procedures, or behavioral strategies being tested and how they are applied within this trial.
Transcutaneous Carbon Dioxide Monitoring
Once an infant is identified as being eligible for TH treatment and hypothermia was initiated according to the department clinical practice guidelines, and written informed consent was obtained from one of the parents, tcPCO2 monitoring can be started. Transcutaneous CO2 will be measured by SenTec Digital Monitor (software version SW-V07.00; MPB SW-V05.00.12) with V-Sign™ Sensor (SenTec AG, Thervil, Switzerland). Also, we will use small blood samples (0.2 ml) from clinical blood draws up to 4 times following starting transcutaneous CO2 monitoring for measuring blood gas for research purposes.
Intervention Type
DEVICE
Eligibility Criteria
Check the participation requirements, including inclusion and exclusion rules, age limits, and whether healthy volunteers are accepted.
Inclusion Criteria
Current criteria for therapeutic hypothermia at BWH include the following:
1. ≥34 weeks' gestation
\+
2. Any one of the followings
1. Sentinel event prior to delivery
2. Apgar score ≤ 5 at 10 min
3. Requires PPV, Intubation or CPR at 10 min
4. pH ≤ 7.1 (from cord or blood gas within 60 min of birth) e. Abnormal Base Excess ≤ - 10 mEq/L (from cord or blood gas within 60 min of birth) +
3. Any one of the followings:
1. Neonatal Encephalopathy Scale Exam Score ≥4
2. Seizure or clinical concern for seizure
1. ≥34 weeks' gestation
\+
2. Any one of the followings
1. Sentinel event prior to delivery
2. Apgar score ≤ 5 at 10 min
3. Requires PPV, Intubation or CPR at 10 min
4. pH ≤ 7.1 (from cord or blood gas within 60 min of birth) e. Abnormal Base Excess ≤ - 10 mEq/L (from cord or blood gas within 60 min of birth) +
3. Any one of the followings:
1. Neonatal Encephalopathy Scale Exam Score ≥4
2. Seizure or clinical concern for seizure
Exclusion Criteria
1. Infants with major birth defect, genetic or metabolic syndrome
2. Neonates in extremis with possibility of redirection to palliative care
2. Neonates in extremis with possibility of redirection to palliative care
Minimum Eligible Age
0 Days
Maximum Eligible Age
3 Days
Eligible Sex
ALL
Accepts Healthy Volunteers
No
Sponsors
Meet the organizations funding or collaborating on the study and learn about their roles.
Medtronic
INDUSTRY
Sponsor Role
collaborator
Brigham and Women's Hospital
OTHER
Sponsor Role
lead
Responsible Party
Identify the individual or organization who holds primary responsibility for the study information submitted to regulators.
Mohamed El-Dib, MD
Principal Investigator
Responsibility Role
PRINCIPAL_INVESTIGATOR
Principal Investigators
Learn about the lead researchers overseeing the trial and their institutional affiliations.
Mohamed El-Dib, MD
Role: PRINCIPAL_INVESTIGATOR
Brigham and Women's Hospital
Locations
Explore where the study is taking place and check the recruitment status at each participating site.
Brigham and Women's Hospital
Boston, Massachusetts, United States
Site Status
Countries
Review the countries where the study has at least one active or historical site.
United States
References
Explore related publications, articles, or registry entries linked to this study.
Nadeem M, Murray D, Boylan G, Dempsey EM, Ryan CA. Blood carbon dioxide levels and adverse outcome in neonatal hypoxic-ischemic encephalopathy. Am J Perinatol. 2010 May;27(5):361-5. doi: 10.1055/s-0029-1243309. Epub 2009 Dec 10.
Reference Type
BACKGROUND
Edwards AD, Brocklehurst P, Gunn AJ, Halliday H, Juszczak E, Levene M, Strohm B, Thoresen M, Whitelaw A, Azzopardi D. Neurological outcomes at 18 months of age after moderate hypothermia for perinatal hypoxic ischaemic encephalopathy: synthesis and meta-analysis of trial data. BMJ. 2010 Feb 9;340:c363. doi: 10.1136/bmj.c363.
Reference Type
BACKGROUND
Jacobs SE, Berg M, Hunt R, Tarnow-Mordi WO, Inder TE, Davis PG. Cooling for newborns with hypoxic ischaemic encephalopathy. Cochrane Database Syst Rev. 2013 Jan 31;2013(1):CD003311. doi: 10.1002/14651858.CD003311.pub3.
Reference Type
BACKGROUND
Kurinczuk JJ, White-Koning M, Badawi N. Epidemiology of neonatal encephalopathy and hypoxic-ischaemic encephalopathy. Early Hum Dev. 2010 Jun;86(6):329-38. doi: 10.1016/j.earlhumdev.2010.05.010. Epub 2010 Jun 16.
Reference Type
BACKGROUND
Pappas A, Shankaran S, Laptook AR, Langer JC, Bara R, Ehrenkranz RA, Goldberg RN, Das A, Higgins RD, Tyson JE, Walsh MC; Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network. Hypocarbia and adverse outcome in neonatal hypoxic-ischemic encephalopathy. J Pediatr. 2011 May;158(5):752-758.e1. doi: 10.1016/j.jpeds.2010.10.019. Epub 2010 Dec 10.
Reference Type
BACKGROUND
Laffey JG, Kavanagh BP. Hypocapnia. N Engl J Med. 2002 Jul 4;347(1):43-53. doi: 10.1056/NEJMra012457. No abstract available.
Reference Type
BACKGROUND
Yenari MA, Han HS. Neuroprotective mechanisms of hypothermia in brain ischaemia. Nat Rev Neurosci. 2012 Feb 22;13(4):267-78. doi: 10.1038/nrn3174.
Reference Type
BACKGROUND
Klinger G, Beyene J, Shah P, Perlman M. Do hyperoxaemia and hypocapnia add to the risk of brain injury after intrapartum asphyxia? Arch Dis Child Fetal Neonatal Ed. 2005 Jan;90(1):F49-52. doi: 10.1136/adc.2003.048785.
Reference Type
BACKGROUND
Lingappan K, Kaiser JR, Srinivasan C, Gunn AJ. Relationship between PCO2 and unfavorable outcome in infants with moderate-to-severe hypoxic ischemic encephalopathy. Pediatr Res. 2016 Aug;80(2):204-8. doi: 10.1038/pr.2016.62. Epub 2016 Apr 6.
Reference Type
BACKGROUND
Lopez Laporte MA, Wang H, Sanon PN, Barbosa Vargas S, Maluorni J, Rampakakis E, Wintermark P. Association between hypocapnia and ventilation during the first days of life and brain injury in asphyxiated newborns treated with hypothermia. J Matern Fetal Neonatal Med. 2019 Apr;32(8):1312-1320. doi: 10.1080/14767058.2017.1404980. Epub 2017 Nov 27.
Reference Type
BACKGROUND
Curley G, Laffey JG, Kavanagh BP. Bench-to-bedside review: carbon dioxide. Crit Care. 2010;14(2):220. doi: 10.1186/cc8926. Epub 2010 Apr 30.
Reference Type
BACKGROUND
Greisen G. Autoregulation of cerebral blood flow in newborn babies. Early Hum Dev. 2005 May;81(5):423-8. doi: 10.1016/j.earlhumdev.2005.03.005.
Reference Type
BACKGROUND
Greisen G, Munck H, Lou H. Severe hypocarbia in preterm infants and neurodevelopmental deficit. Acta Paediatr Scand. 1987 May;76(3):401-4. doi: 10.1111/j.1651-2227.1987.tb10489.x.
Reference Type
BACKGROUND
Tingay DG, Stewart MJ, Morley CJ. Monitoring of end tidal carbon dioxide and transcutaneous carbon dioxide during neonatal transport. Arch Dis Child Fetal Neonatal Ed. 2005 Nov;90(6):F523-6. doi: 10.1136/adc.2004.064717. Epub 2005 Apr 29.
Reference Type
BACKGROUND
Sandberg KL, Brynjarsson H, Hjalmarson O. Transcutaneous blood gas monitoring during neonatal intensive care. Acta Paediatr. 2011 May;100(5):676-9. doi: 10.1111/j.1651-2227.2011.02164.x. Epub 2011 Feb 14.
Reference Type
BACKGROUND
Hejlesen OK, Cichosz SL, Vangsgaard S, Andresen MF, Madsen LP. Clinical implications of a quality assessment of transcutaneous CO2 monitoring in preterm infants in neonatal intensive care. Stud Health Technol Inform. 2009;150:490-4.
Reference Type
BACKGROUND
Aly S, El-Dib M, Mohamed M, Aly H. Transcutaneous Carbon Dioxide Monitoring with Reduced-Temperature Probes in Very Low Birth Weight Infants. Am J Perinatol. 2017 Apr;34(5):480-485. doi: 10.1055/s-0036-1593352. Epub 2016 Sep 27.
Reference Type
BACKGROUND
Mukhopadhyay S, Maurer R, Puopolo KM. Neonatal Transcutaneous Carbon Dioxide Monitoring--Effect on Clinical Management and Outcomes. Respir Care. 2016 Jan;61(1):90-7. doi: 10.4187/respcare.04212. Epub 2015 Oct 27.
Reference Type
BACKGROUND
Restrepo RD, Hirst KR, Wittnebel L, Wettstein R. AARC clinical practice guideline: transcutaneous monitoring of carbon dioxide and oxygen: 2012. Respir Care. 2012 Nov;57(11):1955-62. doi: 10.4187/respcare.02011.
Reference Type
BACKGROUND
Sorensen LC, Brage-Andersen L, Greisen G. Effects of the transcutaneous electrode temperature on the accuracy of transcutaneous carbon dioxide tension. Scand J Clin Lab Invest. 2011 Nov;71(7):548-52. doi: 10.3109/00365513.2011.590601. Epub 2011 Jul 6.
Reference Type
BACKGROUND
Chalak LF, Tarumi T, Zhang R. The "neurovascular unit approach" to evaluate mechanisms of dysfunctional autoregulation in asphyxiated newborns in the era of hypothermia therapy. Early Hum Dev. 2014 Oct;90(10):687-94. doi: 10.1016/j.earlhumdev.2014.06.013. Epub 2014 Jul 23.
Reference Type
BACKGROUND
Vanderhaegen J, Naulaers G, Vanhole C, De Smet D, Van Huffel S, Vanhaesebrouck S, Devlieger H. The effect of changes in tPCO2 on the fractional tissue oxygen extraction--as measured by near-infrared spectroscopy--in neonates during the first days of life. Eur J Paediatr Neurol. 2009 Mar;13(2):128-34. doi: 10.1016/j.ejpn.2008.02.012. Epub 2008 Jul 10.
Reference Type
BACKGROUND
Dix LML, Weeke LC, de Vries LS, Groenendaal F, Baerts W, van Bel F, Lemmers PMA. Carbon Dioxide Fluctuations Are Associated with Changes in Cerebral Oxygenation and Electrical Activity in Infants Born Preterm. J Pediatr. 2017 Aug;187:66-72.e1. doi: 10.1016/j.jpeds.2017.04.043. Epub 2017 May 31.
Reference Type
BACKGROUND
Lasso Pirot A, Fritz KI, Ashraf QM, Mishra OP, Delivoria-Papadopoulos M. Effects of severe hypocapnia on expression of bax and bcl-2 proteins, DNA fragmentation, and membrane peroxidation products in cerebral cortical mitochondria of newborn piglets. Neonatology. 2007;91(1):20-7. doi: 10.1159/000096967. Epub 2007 Nov 10.
Reference Type
BACKGROUND
Provided Documents
Download supplemental materials such as informed consent forms, study protocols, or participant manuals.
Document Type: Study Protocol
Document Type: Informed Consent Form
Other Identifiers
Review additional registry numbers or institutional identifiers associated with this trial.
2019P001572
Identifier Type: -
Identifier Source: org_study_id
More Related Trials
Additional clinical trials that may be relevant based on similarity analysis.
Enteral Feeding and Splanchnic NIRS Values in Infants With Neonatal Encephalopathy (NE)
NCT05471336
COMPLETED
NA
Delayed Cord Clamping With Oxygen In Extremely Low Gestation Infants
NCT04413097
ACTIVE_NOT_RECRUITING
NA
Optimizing (Longer, Deeper) Cooling for Neonatal Hypoxic-Ischemic Encephalopathy(HIE)
NCT01192776
TERMINATED
NA
Impact of Different Modes of Noninvasive Ventilation on Regional Oximetry and Hemodynamics in Premature Newborn
NCT01942967
COMPLETED
Quantitative End Tidal CO2 Monitoring in the Delivery Room (DR)
NCT01381068
COMPLETED
NA
Real-time State of Vigilance Monitor for the Neonatal Intensive Care Unit
NCT04920175
COMPLETED
Successful Extubation and Noninvasive Ventilation in Preterm ≤ 1500g Terms
NCT02396693
COMPLETED
NA
Correlation of CO2 Measured by Blood Gas vs Transcutaneous Monitor
NCT03268395
UNKNOWN
NA
Hypothermia Prevention in Low Birthweight and Preterm Infants
NCT04364204
UNKNOWN
NA
Comparison of Different Oxygen Delivery Strategies During Resuscitation of Babies
NCT00356902
COMPLETED
NA
Comparative Outcomes Related to Delivery-room Cord Milking In Low-resourced Kountries
NCT03657394
ACTIVE_NOT_RECRUITING
NA
Neonatal Warming to Prevent Hypothermia
NCT04827394
COMPLETED
NA
Pilot Study to Assess Safety and Feasibility of Resuscitation of Preterm Infants With Controlled Volume of Air/Oxygen
NCT00157989
TERMINATED
PHASE3
Use of CO2 Detectors to Help Provide Effective Breaths During Resuscitation of Preterm Newborns
NCT04287907
COMPLETED
NA
Nasal High Frequency Oscillatory Versus Nasal Intermittent Positive Pressure Ventilation in Neonate After Extubation
NCT02543125
UNKNOWN
NA
Neonatal Wireless Monitoring System for Intensive Care
NCT04241263
UNKNOWN
NA
Effects of Two Modalities of Non-invasive Ventilation After Extubation in Very Low Birth Weight Neonates
NCT03551314
COMPLETED
NA
Neurodevelopmental Outcome in Newborn With Hypoxic-ischemic Encephalopathy Treated With Therapeutic Hypothermia
NCT05767476
RECRUITING
Repercussions of Respiratory Physiotherapy in Preterm Infants Under Mechanical Ventilation
NCT03159039
COMPLETED
NA
Optimising the Duration of Cooling in Mild Encephalopathy
NCT03409770
UNKNOWN
NA
Long Term Prognostic of Neonatal Hypoxic Ischemic Encephalopathy With Hypothermia Treatment
NCT02676063
UNKNOWN
Early or Late Cord Clamping in the Depressed Neonate
NCT02727517
COMPLETED
NA
The Impact of Continuous Transcutaneous CO2 (TCCO2) Monitoring in Extremely Low Birth Weight (ELBW) Infants
NCT03477708
COMPLETED
Heart Rate Evaluation and Resuscitation Trial in Preterm Neonates
NCT03133663
COMPLETED
NA
Evaluation of Use of Plastic Bags to Prevent Neonatal Hypothermia-Part V
NCT01604460
COMPLETED
PHASE4