Dexmedetomidine and Subarachnoid Haemorrhage
The purpose of this study is to investigate how dexmedetomidine affects static and dynamic autoregulation, intracranial pressure (ICP) and cerebral oxygenation in aneurysmal subarachnoid haemorrhage (SAH) patients.
Drug: Dexmedetomidine infusion
|Study Design:||Endpoint Classification: Safety Study
Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Basic Science
|Official Title:||The Effects of Dexmedetomidine on Cerebral Autoregulation and Cerebral Oxygenation in Subarachnoid Haemorrhage Patients|
- Change in autoregulation, ICP and cerebral oxygenation [ Time Frame: 2, 4 and 6 hours ] [ Designated as safety issue: Yes ]Autoregulation is assessed using transcranial doppler (TCD) and ICP amplitude analysis. ICP and cerebral oxygenation are part of standard multimodal monitoring and these are continuously monitored and recorded.
|Experimental: Dexmedetomine infusion||
Drug: Dexmedetomidine infusion
Both static and dynamic autoregulation are assessed first during propofol infusion, before commencement of dexmedetomidine infusion. Dexmedetomidine infusion is commenced with a dose of 0.7 μg/kg/h and propofol infusion is stopped concomitantly. After 2 hours dexmedetomidine infusion, the static and dynamic autoregulation are assessed. If there are no signs of worsening of autoregulation, then the dexmedetomidine infusion is increased to 1 μg/kg/h and after 2 hours the static and dynamic autoregulation are assessed again. However, if autoregulation worsens during dexmedetomidine infusion, it will be stopped and further testing with dexmedetomidine will not be carried out. If autoregulation does not worsen with the 1 μg/kg/h dose then the dose will be increased to 1.4 μg/kg/h. After 2 hours infusion the dynamic and static autoregulation are assessed again.
Blood samples for determining dexmedetomidine plasma concentration are collected alongside with the autoregulation assessments
Dexmedetomidine is a selective α2-agonist which induces sedation, anxiolysis and analgesia without respiratory depression. These effects, as well as neuroprotective properties in experimental studies would be ideal in neuroanaesthesia and in neurocritical care. Poor grade SAH patients are treated in intensive care units (ICU). These patients are sedated often with propofol. However, to assess the patient's neurology, the propofol sedation must be stopped and the wakening of the patient may take time. Dexmedetomidine would be more advantageous, allowing wakening during the infusion. However, the effects of dexmedetomidine on cerebral autoregulation are unknown in SAH patients.
15 SAH patients requiring sedation, mechanical ventilation and ICP monitoring will be rolled in to the study.
|Contact: Riikka SK Takala, MD PhDfirstname.lastname@example.org|
|Contact: Minna Kallioinen, MDemail@example.com|
|Turku University Hospital||Not yet recruiting|
|Turku, Finland, 20520|
|Contact: Riikka SK Takala, MD PhD firstname.lastname@example.org|
|Principal Investigator: Minna Kallioinen, MD|
|Principal Investigator: Ari J Katila, MD|
|Study Director:||Riikka SK Takala, MD PhD||Turku University Hospital|