Hypoxic Ischemic Encephalopathy (HIE)NCT06694545
Neonates With Hypoxic Ischemic Encephalopathy (HIE)
An observational study of Hypoxic Ischemic Encephalopathy (HIE), run by Assiut University.
Trial summary
Assessment of the potential neuroprotective effect of magnesium sulphate and caffeine in treating asphyxiated newborns and improvement of the neurological outcome of Hypoxic Ischemic Encephalopathy in Assiut university hospital of Children Read more about this study
- Who is it for?
- Ages 1 day to 28 days
- Conditions the study is for
- Hypoxic Ischemic Encephalopathy (HIE)
- How many people
- 72 participants
- Where
- No sites listed yet
- Study dates
- 1 Dec 2024to 31 Jan 2026
- Phase
- Observational
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 1 day to 28 days
- All sexes
- No healthy volunteers
- Child
Study population: Neonates with Hypoxic Ischemic Encephalopathy (HIE) .Encephalopathy in neonates is broadly defined brain dysfunction in a newborn manifesting as alteration in mental status and abnormal neurologic examination. Neonatal encephalopathy (NE) may result from acute or chronic hypoxic-ischemic injury, brain malformations, vascular injuries (including stroke), inborn errors of metabolism, and other causes. Hypoxic-ischemic encephalopathy (HIE) is a specific diagnosis and applies only when a neonate has encephalopathy that is known or highly suspected to be due to a hypoxic-ischemic event.
Who may be able to join
- Neonates with suspected perinatal asphyxia APGAR score < 3 at 5 min.
- Neonates whose mother did not receive MgSO4 or caffeine
Who cannot join
- Neonates with Apgar's score > 3 at 5 min
- Neonates with congenital malformations
- Neonates whose mother had general anasthesia
Trial locations and contacts
No sites are listed yet. Contact the study team or a site near you to ask about taking part.
About this study
Official title: Role of Intravenous Magnesium Sulphate and Caffeine in Neonates With Hypoxic Ischemic Encephalopathy (HIE) in a Assiut University Hospital of Children
Assessment of the potential neuroprotective effect of magnesium sulphate and caffeine in treating asphyxiated newborns and improvement of the neurological outcome of Hypoxic Ischemic Encephalopathy in Assiut university hospital of Children
Read the detailed description
Encephalopathy in neonates is broadly defined as brain dysfunction in a newborn manifesting as alteration in mental status and abnormal neurologic examination. Neonatal encephalopathy (NE) may result from acute or chronic hypoxic-ischemic injury, brain malformations, vascular injuries (including stroke), inborn errors of metabolism, and other causes. Hypoxic-ischemic encephalopathy (HIE) is a specific diagnosis and applies only when a neonate has encephalopathy that is known or highly suspected to be due to a hypoxic-ischemic event.
Perinatal asphyxia is a condition where hypoxaemia and acidosis are present in the fetus or the newborn infants. It is a failure newborn to initiate spontaneous, sustained, and vigorous respiration effort at birth. It is also defined as a failure to initiate spontaneous respirations and/or a 5-minute Apgar score of less than 7: the most commonly used indicator in the identification of birth asphyxia in resource limited settings . About 20% - 30% of asphyxiated newborns who develop hypoxic ischemic encephalopathy (HIE) die during the neonatal period, and one third to one half of survivors are left with cerebral palsy and mental retardation . Survivors present with several short and long term morbidities, including: seizure disorders, tone abnormalities, feeding difficulties, delayed developmental milestones, learning difficulties, cerebral palsy and mental retardation. The frequency of severe perinatal asphyxia complications, hypoxic ischemic encephalopathy (HIE) and incidence of up to 26.5/1000 live births is unacceptably high despite advances in perinatal care . Encephalopathy occurs in 50% to 60% of patients with severe perinatal asphyxia. Among patients with moderate HIE, 10% to 20% die, and 30% to 40% develop neurodevelopmental disorders, whereas 50% of patients with severe HIE die and almost all survivors develop neurodevelopmental deficits Neuro-science research has revealed our understanding of the mechanisms by perinatal asphyxia neuronal damage and adverse consequences. Asphyxia leads to two types of cerebral injuries: the primary neuronal injury that occurs at the time of hypoxic-ischemic insults and the secondary cerebral injury that occurs over hours to days after accumulation of excessive intra-neuronal calcium through stimulation of the excitatory N-methyl-D-aspartate (NMDA) glutamate receptors, which triggers apoptosis of the affected neurons . Magnesium is a naturally occurring NMDA receptor antagonist that blocks neuronal influx of calcium within the ion channels. This block is voltage-dependent and is overcome during axonal depolarization that occurs in hypoxic-ischemic insults. If the extra-cellular magnesium concentration is increased, this blockade can be restored. Magnesium sulphate may also have direct actions on mitochondrial activity, anticonvulsant properties and hemodynamic effects by increasing cerebral blood flow. Some data also suggest that MgSO4 may serve an anti-apoptotic role and prevent neuronal cell loss .
Clinical studies have shown that caffeine also has neuroprotective effects in premature infants by alleviating hypoxia induced white matter damage, and improving ventilation function and brain self-regulation In addition, caffeine has been shown to reduce the apoptosis of developing brain neurons, ventricular enlargement, and white matter loss caused by hypoxia.
- Conditions
- Hypoxic Ischemic Encephalopathy (HIE)
- Medical subject headings
- Hypoxia-Ischemia, Brain
What is being measured
The primary outcome is the main question the study is designed to answer.
Assessment of the potential neuroprotective effect of magnesium sulphate and caffeine in improvement of the neurological outcome of hypoxic ischemic encephalopathy in Assuit university hospital.
Assesment of neuroprotective effect of magnesium sulphate and caffeine by :
- Determine the benefit of magnesium sulphate and caffeine on perinatal asphyxia.
- Determine the effect of magnesium sulphate and caffeine on neurological outcome in severe perinatal Asphyxia.
- Determine the effect of magnesium sulphate and caffeine on reduction of duration of Admission/hospitalization.
Measured: Baseline
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted19 Nov 2024
- Study start1 Dec 2024 (estimated)
- Primary completion31 Dec 2025 (estimated)
- Study completion31 Jan 2026 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (3)Papers the sponsor has linked to this study.
- Other trials for Hypoxic Ischemic Encephalopathy (HIE)Studies of the same condition, open and under way.
- More trials run by Assiut UniversityThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 72 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Assiut University
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Andrew Malak Zaki Malak, Assiut University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06694545
- Sponsor's protocol ID
- Hypoxic IschemicEncephalopathy
- Status last verified
- Nov 2024
- First submitted
- 6 Sep 2024
- Last updated
- 19 Nov 2024
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Azra Haider B, Bhutta ZA. Birth asphyxia in developing countries: current status and public health implications. Curr Probl Pediatr Adolesc Health Care. 2006 May-Jun;36(5):178-88. doi: 10.1016/j.cppeds.2005.11.002. No abstract available.
PubMed 16631096Chalak L, Ferriero DM, Gressens P, Molloy E, Bearer C. A 20 years conundrum of neonatal encephalopathy and hypoxic ischemic encephalopathy: are we closer to a consensus guideline? Pediatr Res. 2019 Nov;86(5):548-549. doi: 10.1038/s41390-019-0547-9. Epub 2019 Aug 26. No abstract available.
PubMed 31450231Volpe JJ. Neonatal encephalopathy: an inadequate term for hypoxic-ischemic encephalopathy. Ann Neurol. 2012 Aug;72(2):156-66. doi: 10.1002/ana.23647.
PubMed 22926849
Study at a glance
From the registry record, last updated by the sponsor on 19 Nov 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Role of Intravenous Magnesium Sulphate and Caffeine in Neonates With Hypoxic Ischemic Encephalopathy (HIE) in a Assiut University Hospital of Children
- ClinicalTrials.gov ID
- NCT06694545
- Acronym / sponsor ID
- Hypoxic IschemicEncephalopathy
- Conditions
- Hypoxic Ischemic Encephalopathy (HIE)
- Study type
- Observational
- Recruitment status
- Not yet recruiting
- Enrolment
- 72 participants (estimated)
- Lead sponsor
- Assiut UniversityUniversity, hospital or other
- Study start
- 1 Dec 2024 (estimated)
- Primary completion
- 31 Dec 2025 (estimated)
- Study completion
- 31 Jan 2026 (estimated)
- First posted
- 19 Nov 2024 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Assessment of the potential neuroprotective effect of magnesium sulphate and caffeine in treating asphyxiated newborns and improvement of the neurological outcome of Hypoxic Ischemic Encephalopathy in Assiut university hospital of Children
Detailed description
Encephalopathy in neonates is broadly defined as brain dysfunction in a newborn manifesting as alteration in mental status and abnormal neurologic examination. Neonatal encephalopathy (NE) may result from acute or chronic hypoxic-ischemic injury, brain malformations, vascular injuries (including stroke), inborn errors of metabolism, and other causes. Hypoxic-ischemic encephalopathy (HIE) is a specific diagnosis and applies only when a neonate has encephalopathy that is known or highly suspected to be due to a hypoxic-ischemic event.
Perinatal asphyxia is a condition where hypoxaemia and acidosis are present in the fetus or the newborn infants. It is a failure newborn to initiate spontaneous, sustained, and vigorous respiration effort at birth. It is also defined as a failure to initiate spontaneous respirations and/or a 5-minute Apgar score of less than 7: the most commonly used indicator in the identification of birth asphyxia in resource limited settings . About 20% - 30% of asphyxiated newborns who develop hypoxic ischemic encephalopathy (HIE) die during the neonatal period, and one third to one half of survivors are left with cerebral palsy and mental retardation . Survivors present with several short and long term morbidities, including: seizure disorders, tone abnormalities, feeding difficulties, delayed developmental milestones, learning difficulties, cerebral palsy and mental retardation. The frequency of severe perinatal asphyxia complications, hypoxic ischemic encephalopathy (HIE) and incidence of up to 26.5/1000 live births is unacceptably high despite advances in perinatal care . Encephalopathy occurs in 50% to 60% of patients with severe perinatal asphyxia. Among patients with moderate HIE, 10% to 20% die, and 30% to 40% develop neurodevelopmental disorders, whereas 50% of patients with severe HIE die and almost all survivors develop neurodevelopmental deficits Neuro-science research has revealed our understanding of the mechanisms by perinatal asphyxia neuronal damage and adverse consequences. Asphyxia leads to two types of cerebral injuries: the primary neuronal injury that occurs at the time of hypoxic-ischemic insults and the secondary cerebral injury that occurs over hours to days after accumulation of excessive intra-neuronal calcium through stimulation of the excitatory N-methyl-D-aspartate (NMDA) glutamate receptors, which triggers apoptosis of the affected neurons . Magnesium is a naturally occurring NMDA receptor antagonist that blocks neuronal influx of calcium within the ion channels. This block is voltage-dependent and is overcome during axonal depolarization that occurs in hypoxic-ischemic insults. If the extra-cellular magnesium concentration is increased, this blockade can be restored. Magnesium sulphate may also have direct actions on mitochondrial activity, anticonvulsant properties and hemodynamic effects by increasing cerebral blood flow. Some data also suggest that MgSO4 may serve an anti-apoptotic role and prevent neuronal cell loss .
Clinical studies have shown that caffeine also has neuroprotective effects in premature infants by alleviating hypoxia induced white matter damage, and improving ventilation function and brain self-regulation In addition, caffeine has been shown to reduce the apoptosis of developing brain neurons, ventricular enlargement, and white matter loss caused by hypoxia.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
Who may qualify
- Ages
- 1 day to 28 days
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child
- Study population
- Neonates with Hypoxic Ischemic Encephalopathy (HIE) .Encephalopathy in neonates is broadly defined brain dysfunction in a newborn manifesting as alteration in mental status and abnormal neurologic examination. Neonatal encephalopathy (NE) may result from acute or chronic hypoxic-ischemic injury, brain malformations, vascular injuries (including stroke), inborn errors of metabolism, and other causes. Hypoxic-ischemic encephalopathy (HIE) is a specific diagnosis and applies only when a neonate has encephalopathy that is known or highly suspected to be due to a hypoxic-ischemic event.
Key inclusion criteria (2 listed)
- Neonates with suspected perinatal asphyxia APGAR score < 3 at 5 min.
- Neonates whose mother did not receive MgSO4 or caffeine
Key exclusion criteria (3 listed)
- Neonates with Apgar's score > 3 at 5 min
- Neonates with congenital malformations
- Neonates whose mother had general anasthesia
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Assessment of the potential neuroprotective effect of magnesium sulphate and caffeine in improvement of the neurological outcome of hypoxic ischemic encephalopathy in Assuit university hospital.
Time frame: Baseline
Assesment of neuroprotective effect of magnesium sulphate and caffeine by : 1. Determine the benefit of magnesium sulphate and caffeine on perinatal asphyxia. 2. Determine the effect of magnesium sulphate and caffeine on neurological outcome in severe perinatal Asphyxia. 3. Determine the effect of magnesium sulphate and caffeine on reduction of duration of Admission/hospitalization.
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 19 Nov 2024.
- Results publication: PubMed 16631096Azra Haider B, Bhutta ZA. Birth asphyxia in developing countries: current status and public health implications. Curr Probl Pediatr Adolesc Health Care. 2006 May-Jun;36(5):178-88. doi: 10.1016/j.cppeds.2005.11.002. No abstract available.
- Results publication: PubMed 31450231Chalak L, Ferriero DM, Gressens P, Molloy E, Bearer C. A 20 years conundrum of neonatal encephalopathy and hypoxic ischemic encephalopathy: are we closer to a consensus guideline? Pediatr Res. 2019 Nov;86(5):548-549. doi: 10.1038/s41390-019-0547-9. Epub 2019 Aug 26. No abstract available.
- Results publication: PubMed 22926849Volpe JJ. Neonatal encephalopathy: an inadequate term for hypoxic-ischemic encephalopathy. Ann Neurol. 2012 Aug;72(2):156-66. doi: 10.1002/ana.23647.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part.
Questions about this trial
What is this clinical trial studying?
An observational study of Hypoxic Ischemic Encephalopathy (HIE), run by Assiut University.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 2 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: opening soon, as of the sponsor's last update on 19 Nov 2024. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Andrew Malak Zaki (01211843381, Andria.16266283@med.aun.edu.eg), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Assessment of the potential neuroprotective effect of magnesium sulphate and caffeine in improvement of the neurological outcome of hypoxic ischemic encephalopathy in Assuit university hospital. (time frame: Baseline). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT06694545, which also lists 3 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 19 Nov 2024.