Acute rupture of cerebral aneurysm, subarachnoid hemorrhage (SAH), unconsciousness, brain injury. MedDRA version: 20.1 Level: LLT Classification code 10008078 Term: Cerebral arterial aneurysm System Organ Class: 100000004852
Conditions
Interventions
Trade Name: Xenon pro Anesthesia
Product Name: Xenon pro Anesthesia
Pharmaceutical Form: Medicinal gas, liquefied
Trade Name: Conoxia (Air/Oxygen with at least 21% oxygen)
Product Name: Conoxia
Pharm
Sponsors
Timo Laitio
Eligibility
Sex/Gender
All
Inclusion criteria
Inclusion criteria: 1. Aneurysmal subarachnoid hemorrhage visible on CTA or DSA. 2. Hunt-Hess 3-5 3. Age of = 18 years 4. Intubated. 5. GCS 3–12 obtained off neuromuscular blocking agents 6. Xenon treatment started within 6 hours after onset of SAH symptoms Are the trial subjects under 18? no Number of subjects for this age range: F.1.2 Adults (18-64 years) yes F.1.2.1 Number of subjects for this age range 140 F.1.3 Elderly (>=65 years) yes F.1.3.1 Number of subjects for this age range 20
Exclusion criteria
Exclusion criteria: 1. Acute traumatic brain injury 2. Maximum diameter of intracerebral hemorrhage > 2.5 cm 3. Pneumothorax or pneumomediastinum, 4. Acute lung injury requiring = 60% FIO2 (fraction of inspired oxygen). 5. Systolic arterial pressure < 80 mmHg or mean arterial pressure < 60 mmHg for over 30 min period 6. Bilaterally fixed and dilated pupils 7. Positive pregnancy test, known pregnancy, or current breast-feeding 8. Chronic neurological deficiency due to chronic traumatic brain injury or other neurological illness 9. Imminent death or current life-threatening disease 10. Current enrollment in another interventional study 11. The subject is known to have a clinically significant laboratory abnormality, medical condition (such as decompensated liver disease or severe chronic obstructive pulmonary disease), or social circumstance that, in the investigator’s opinion, makes it inappropriate for the subject to participate in this clinical trial. 12. Presence of implants or foreign bodies which are not known to be MRI safe
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| Main Objective: Main Objective: To explore neuroprotective properties of xenon in patients after aneurysmal subarachnoid hemorrhage (SAH). Primary endpoint: Global fractional anisotropy of white matter of diffusion tensor imaging (DTI). Hypothesis: White matter damage is less severe in xenon treated patients, i.e. global fractional anisotropy is significantly higher in the xenon group than in the control group as assessed with the 1st MRI within 48-96 hours after onset of SAH symptoms.;Secondary Objective: Fractional anisotropy of white matter at cerebellum and/or at corpus callosum. Exploratory endpoints: 1. Composite of radiological EBI (i.e. the 1st MRI) and DCI (Criterion of DCI: 1. a new focal neurological deficit/decrease in level of consciousness not due to other causes, e.g. hydrocephalus, seizures, metabolic derangement, infection, sedation, 2. a new infarct on follow-up imaging after 4 days post-SAH, i.e. 2nd MRI, or 3. both 1 and 2), and poor outcome (good: mRS 0-2; poor: mRS 3-6) at 3-months and at 1 year. 3. Neurogenic Stress Cardiomyopathy and Stunned Myocardium. 4 Need for ICP therapies (hypothermia, decompressive craniotomy); 8. Development of prognostication models for EBI and DCI and long-term outcome at 1 and 2 years after SAH by combining data of brain imaging, clinical data (including Turku Aneurysm Data) and metabolomics; 11. Activity of microglia cells;Primary end point(s): Global fractional anisotropy of white matter of diffusion tensor imaging (DTI). Hypothesis: White matter damage is less severe in xenon treated patients, i.e. global fractional anisotropy is significantly higher in the xenon group than in the control group as assessed with the 1st MRI within 48-96 hours after onset of SAH symptoms.;Timepoint(s) of evaluation of this end point: 48-96 hours after onset of SAH symptoms. | — |
Secondary
| Measure | Time frame |
|---|---|
| Secondary end point(s): Fractional anisotropy of white matter at cerebellum and/or at corpus callosum Exploratory endpoints: 1. Composite of radiological EBI (i.e. the 1st MRI) and DCI (Criterion of DCI: 1. a new focal neurological deficit/decrease in level of consciousness not due to other causes, e.g. hydrocephalus, seizures, metabolic derangement, infection, sedation, 2. a new infarct on follow-up imaging after 4 days post-SAH, i.e. 2nd MRI, or 3. both 1 and 2), and poor outcome (good: mRS 0-2; poor: mRS 3-6) at 3-months and at 1 year. 3. Neurogenic Stress Cardiomyopathy and Stunned Myocardium (i.e. myocardial injury caused by sympathetic storm and autonomic dysregulation with hs-troponin elevation, left ventricular dysfunction or ECG changes): 4. ICP level 5. Need for ICP therapies (hypothermia, decompressive craniotomy); 6. Duration of therapy for ICP control/monitoring; 7: Plasma catecholamine level; 8. Development of prognostication models for EBI and DCI and long-term outcome at 1 and 2 years after SAH by combining data of brain imaging, clinical data (including Turku Aneurysm Data) and metabolomics; 9. MRI parameters; 10. Metabolomics of plasma and spinal fluid (i.e. between xenon and control groups, between patients with and without EBI and/or DCI, between survivors and non-survivors at 90 days, at 1 year and at 2 years after onset of SAH symptoms; 11. Activity of microglia cells;Timepoint(s) of evaluation of this end point: During first 6 weeks after onset of SAH symtoms and during a follow-up of one year and at 2 years after onset of SAH symptoms | — |
Countries
Finland
Contacts
Public ContactTurku University Hospital
Timo Laitio
Outcome results
None listed