Clinical Trial Details
— Status: Completed
Administrative data
NCT number |
NCT03724201 |
Other study ID # |
REB18-0409 |
Secondary ID |
|
Status |
Completed |
Phase |
|
First received |
|
Last updated |
|
Start date |
July 30, 2018 |
Est. completion date |
May 1, 2019 |
Study information
Verified date |
December 2023 |
Source |
University of Calgary |
Contact |
n/a |
Is FDA regulated |
No |
Health authority |
|
Study type |
Observational
|
Clinical Trial 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.
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.