Ignite Creation Date:
2024-05-06 @ 12:18 PM
Last Modification Date:
2024-10-26 @ 12:57 PM
Study NCT ID:
NCT03724201
Status:
COMPLETED
Last Update Posted:
2023-12-20
First Post:
2018-10-26
Brief Title:
Neuronal Damage In Delirium Study
Sponsor:
University of Calgary
Organization:
University of Calgary
Study Overview
Official Title:
Delirium Severity Subsyndromal Delirium and Inflammation-associated Biomarkers in Mechanically Ventilated Patients With Sepsis
Status:
COMPLETED
Status Verified Date:
2023-12
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
NDID
Brief Summary:
The purpose of this study is to evaluate associations between neuronal damage biomarkers S100 calcium-binding protein beta S-100β neuron-specific enolase NSE ubiquitin carboxy-terminal hydrolase L1 UCHL1 and brain-derived neurotropic factor BDNF and delirium severity and subsyndromal delirium in a homogeneous population of mechanically ventilated patients with sepsis
Detailed Description:
Due to high levels of inflammation patients with sepsis are especially at risk of developing delirium an organic state of confusion that affects over 80 of mechanically ventilated patients during their intensive care stay A growing body of literature suggests that the severity of delirium symptoms may also have a significant impact on negative outcomes associated with delirium including mortality length of hospital stay duration of mechanical ventilation and functional and cognitive impairment Similarly recent literature suggests that patient outcomes may be worsened by a subthreshold severity level of delirium known as subsyndromal delirium Despite the urgent need to understand delirium and subsyndromal delirium etiology for better detection and management strategies the multifactorial pathophysiology of delirium is still largely unknown Clinical biomarker studies evaluating levels of S100 calcium-binding protein beta S-100β neuron-specific enolase NSE ubiquitin carboxy-terminal hydrolase L1 UCHL1 and brain-derived neurotropic factor BDNF have suggested evidence for their role in delirium pathophysiology but significant associations with delirium severity and subsyndromal delirium have not been reliably established Evaluating the dose-response relationship of S-100β NSE UCHL1 and BDNF with delirium severity and subsyndromal delirium in a homogeneous population of mechanically ventilated patients with sepsis will provide novel insight on the etiological pathway of delirium The investigators will evaluate effect modification and confounding by inflammation and blood-brain barrier permeability by measuring well-established biomarkers interleukin-6 IL-6 and E-selectin respectively Understanding the role of neuronal damage in delirium may be a promising avenue to develop better screening practices and neuroprotective management strategies that may reduce long-term cognitive and functional deficits associated with delirium
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None