Dexmedetomidine and Subarachnoid Haemorrhage

This study is currently recruiting participants. (see Contacts and Locations)
Verified June 2013 by Turku University Hospital
Sponsor:
Collaborator:
Orion Corporation, Orion Pharma
Information provided by (Responsible Party):
Riikka Takala, Turku University Hospital
ClinicalTrials.gov Identifier:
NCT01664520
First received: August 4, 2012
Last updated: August 30, 2013
Last verified: June 2013
  Purpose

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.


Condition Intervention Phase
Subarachnoid Hemorrhage
Aneurysm
Drug: Dexmedetomidine infusion
Phase 1
Phase 2

Study Type: Interventional
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

Resource links provided by NLM:


Further study details as provided by Turku University Hospital:

Primary Outcome Measures:
  • 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.


Estimated Enrollment: 15
Study Start Date: June 2013
Arms Assigned Interventions
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


Detailed Description:

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.

  Eligibility

Ages Eligible for Study:   18 Years to 80 Years
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Criteria

Inclusion Criteria:

  • Aneurysmal SAH
  • Aneurysm treated with coil(s) or clip(s)
  • Age 18-80 years
  • Written informed consent from the next of kin

Exclusion Criteria:

  • Pregnancy
  • Nursing woman
  • Sick sinus syndrome
  • Carotid stenosis
  • Heart rate less than 50 beats / minute
  • Mean arterial pressure less than 50 mmHg
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT01664520

Contacts
Contact: Riikka SK Takala, MD PhD +358405130441 riikka.takala@gmail.com
Contact: Minna Kallioinen, MD minna.kallioinen@tyks.fi

Locations
Finland
Turku University Hospital Recruiting
Turku, Finland, 20520
Contact: Riikka SK Takala, MD PhD       riikka.takala@gmail.com   
Principal Investigator: Minna Kallioinen, MD         
Principal Investigator: Ari J Katila, MD         
Sponsors and Collaborators
Turku University Hospital
Orion Corporation, Orion Pharma
Investigators
Study Director: Riikka SK Takala, MD PhD Turku University Hospital
  More Information

No publications provided

Responsible Party: Riikka Takala, MD, PhD Senior Staff Anaesthesiologist, Turku University Hospital
ClinicalTrials.gov Identifier: NCT01664520     History of Changes
Other Study ID Numbers: Turku University Hospital, 2012-000068-11, KLNRO 45/2012
Study First Received: August 4, 2012
Last Updated: August 30, 2013
Health Authority: Finland: Finnish Medicines Agency

Keywords provided by Turku University Hospital:
Subarachnoid hemorrhage
Dexmedetomidine
Autoregulation
Intracranial pressure
Cerebral oxygenation

Additional relevant MeSH terms:
Hemorrhage
Subarachnoid Hemorrhage
Pathologic Processes
Intracranial Hemorrhages
Cerebrovascular Disorders
Brain Diseases
Central Nervous System Diseases
Nervous System Diseases
Vascular Diseases
Cardiovascular Diseases
Dexmedetomidine
Hypnotics and Sedatives
Central Nervous System Depressants
Physiological Effects of Drugs
Pharmacologic Actions
Central Nervous System Agents
Therapeutic Uses
Analgesics, Non-Narcotic
Analgesics
Sensory System Agents
Peripheral Nervous System Agents
Adrenergic alpha-2 Receptor Agonists
Adrenergic alpha-Agonists
Adrenergic Agonists
Adrenergic Agents
Neurotransmitter Agents
Molecular Mechanisms of Pharmacological Action

ClinicalTrials.gov processed this record on September 16, 2014