Cerebral Desaturation in Traumatic Brain Injury

Brain Injuries Clinical Trial

Official title:

The Incidence and Magnitude of Cerebral Desaturation in Traumatic Brain Injury (TBI) Patients

Clinical Trial Details — Status: Recruiting

Administrative data

• NCT number: NCT02810145
• Other study ID #: HS19659
• Status: Recruiting
• Phase: N/A
• First received: June 20, 2016
• Last updated: October 11, 2016
• Start date: July 2016
• Est. completion date: December 2019

Study information

• Verified date: October 2016
• Source: University of Manitoba
• Contact: Duane J. Funk, MD
• Phone: 204 787-1414
• Email: duane.funk[@]umanitoba.ca
• Is FDA regulated: No
• Health authority: Canada: Ethics Review CommitteeCanada: Institutional Review Board
• Study type: Observational

Clinical Trial Summary

We will determine the incidence and magnitude of cerebral desaturation in TBI. Adult patients (18 years and older) admitted to the Surgical/Trauma Intensive Care Unit (ICU) at the Health Sciences Center with a severe TBI will have cerebral oximetry monitoring instituted within 12 hours of admission and continuing for 72 hours after placement. Decreases in regional cerebral oxygenation will be correlated with ICU hemodynamic parameters including mean arterial pressure, intracranial pressure, and arterial oxygen and carbon dioxide tension.

Description:

In patients who have suffered a traumatic brain injury, the current management strategies focus on the maintenance of normotension and normoxia and a normalized intracranial pressure (ICP). Recent evidence calls into question the utility of ICP monitoring in these patients. More advanced cerebral monitoring such as the use of invasive brain tissue oxygen monitors have not found their way into widespread clinical practice. Cerebral oximetry monitoring utilizes the different absorption characteristics of oxygenated and deoxygenated blood to measure global brain oxygen levels.

While clinicians have no ability to reverse the primary brain injury, they can mitigate the secondary injury effects, namely hypoxia and hypotension. It is well known that maintaining normal blood pressure and oxygen saturation can prevent secondary brain injury. However, it is also known that despite the appearance of normal hemodynamics, brain oxygen delivery in the ischemic penumbra may be inadequate. This secondary brain injury is likely related to decreases in cerebral oxygenation (rSO2).

There have been a number of studies that have examined a link between intraoperative decreases in rSO2 and adverse perioperative outcome. These studies suggest that decreases in rSO2 may be related to both adverse neurologic and non-neurologic sequelae. All of these studies suffer from similar flaws, however. They are typically small in size, have varying definitions of what constitutes a cerebral desaturation event, and have incompletely, or poorly defined complications. Also lacking is a mechanistic explanation for the cerebral desaturations as peripheral oxygen saturation typically remains near normal.

The brain can be considered the organ of highest priority when it comes to tissue hypoperfusion during shock states. When oxygen delivery to the brain is decreased below a critical value, cerebral desaturations occur. In the context of TBI, cerebral desaturation may be the hallmark of secondary injury. Consistent with this hypothesis, in the largest cerebral oximetry trial to date, Murkin and colleagues discovered that the incidence and magnitude of cerebral desaturations was related to major non-neurologic organ morbidity.

Two questions arise in relation to this prior research. First, are these cerebral desaturations causative of the adverse outcomes, and second if these desaturations were treated (i.e. if cerebral oxygenation was normalized) would outcome be improved (i.e. or are cerebral desaturations merely an epiphenomenon)?

This study will determine the incidence and severity of cerebral desaturation in traumatic brain injury patients admitted to the Surgical Intensive Care Unit. We will examine factors associated with cerebral desaturation such as ICP and blood pressure, and will determine if decreases in rSO2 are helpful in prognostication of traumatic brain injury.

Recruitment information / eligibility

• Status: Recruiting
• Enrollment: 30
• Est. completion date: December 2019
• Est. primary completion date: August 2018
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 18 Years and older

Eligibility

Inclusion Criteria:

• Adults 18 years of age or older admitted to ICU with severe TBI (Glasgow coma score <or=8)

Exclusion Criteria:

Study Design

Observational Model: Cohort, Time Perspective: Prospective

Related Conditions & MeSH terms

• Brain Injuries
• Wounds and Injuries

Locations

Country	Name	City	State
Canada	University of Manitoba	Winnipeg	Manitoba

Sponsors (1)

Lead Sponsor	Collaborator
University of Manitoba

Country where clinical trial is conducted

Canada, 

References & Publications (4)

Casati A, Fanelli G, Pietropaoli P, Proietti R, Tufano R, Danelli G, Fierro G, De Cosmo G, Servillo G. Continuous monitoring of cerebral oxygen saturation in elderly patients undergoing major abdominal surgery minimizes brain exposure to potential hypoxia. Anesth Analg. 2005 Sep;101(3):740-7, table of contents. Erratum in: Anesth Analg. 2006 Jun;102(6):1645. Fierro, Giovanni [corrected to Fierro, Giuseppe]. — View Citation

Fischer GW, Lin HM, Krol M, Galati MF, Di Luozzo G, Griepp RB, Reich DL. Noninvasive cerebral oxygenation may predict outcome in patients undergoing aortic arch surgery. J Thorac Cardiovasc Surg. 2011 Mar;141(3):815-21. doi: 10.1016/j.jtcvs.2010.05.017. Epub 2010 Jun 25. — View Citation

Fischer GW. Recent advances in application of cerebral oximetry in adult cardiovascular surgery. Semin Cardiothorac Vasc Anesth. 2008 Mar;12(1):60-9. doi: 10.1177/1089253208316443. Epub 2008 Apr 7. Review. — View Citation

Kazan R, Bracco D, Hemmerling TM. Reduced cerebral oxygen saturation measured by absolute cerebral oximetry during thoracic surgery correlates with postoperative complications. Br J Anaesth. 2009 Dec;103(6):811-6. doi: 10.1093/bja/aep309. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Incidence of cerebral desaturation	The frequency of cerebral desaturation from time of admission to 72 hours post admission to ICU as measured by rSO2 output from cerebral oximetry.	72 hours	No
Primary	Magnitude of cerebral desaturation	The magnitude of cerebral desaturation from time of admission to 72 hours post admission to ICU as measured by rSO2 output from cerebral oximetry.	72 hours	No
Secondary	Association between cerebral desaturation and intracranial pressure	Cerebral desaturation measured by rSO2 output from cerebral oximetry vs intracranial pressure over 72 hours post admission to ICU by an adjusted regression model	72 hours	No
Secondary	Association between cerebral desaturation and mean arterial pressure	Cerebral desaturation measured by rSO2 output from cerebral oximetry vs mean arterial pressure over 72 hours post admission to ICU by an adjusted regression model	72 hours	No
Secondary	Association between cerebral desaturation and arterial oxygenation	Cerebral desaturation measured by rSO2 output from cerebral oximetry vs arterial oxygen tension over 72 hours post admission to ICU by an adjusted regression model	72 hours	No
Secondary	Association between cerebral desaturation and arterial carbon dioxide concentration	Cerebral desaturation measured by rSO2 output from cerebral oximetry vs arterial CO2 over 72 hours post admission to ICU by an adjusted regression model	72 hours	No