Foley Catheter Related Bladder Discomfort (FCRBD): Role of Neutrophil Cells (FCRBD)
|ClinicalTrials.gov Identifier: NCT03118284|
Recruitment Status : Terminated (Principal Investigator is leaving university and halting studies)
First Posted : April 18, 2017
Last Update Posted : November 15, 2018
|Condition or disease||Intervention/treatment|
|Urethra Injury Catheter Site Discomfort||Other: urine collection Other: Blood collection Behavioral: NRS|
Urinary catheterization has been implicated in up to 80% of hospital-acquired UTIs, and has been associated with evidence for immunological and histological damage frequently in the absence of bacteria31. In a recent human study in elderly patients with ASB and UTI analysis of neutrophil activity showed evidence of enzymatic involvement during bladder infection32, and some appeared to relate to pain and inflammation, however no analysis was conducted regarding neutrophil phenotypes and the impact of mtDNA on sterile local injury mediated exclusively by a Foley catheter.
The bladder irritation that results from Foley catheterization appears to be mediated by muscarinic receptors that mediate involuntary bladder smooth-muscle contractility. Thus the main therapy relies on agents with anti-muscarinic activity such as oxybutynin, tolterodine and butylscopolamine, whereas some benefit has been shown with tramadol, ketamine, paracetamol, pregabalin and gabapentin. However no single commonly accepted therapy for FCRBD is available, and there is uncertainty about the safety and efficacy of the current treatments available. Some research has suggested a role for inflammatory mediators in the occurrence of FCRBD as evident by induction of prostaglandin synthesis and cyclooxygenase-2 (COX-2) inhibitors alleviating symptoms related to FCRBD. In summary various therapies to control FCRBD are available but none have directly addressed the acute inflammatory reaction likely mediating these symptoms1,2,3,4. Hence our interest in analyzing the activity of acute inflammatory cells in particular neutrophil activation as a mediator of bladder inflammation and trigger of FCRBD.
Although the exact pathophysiology of FCRBD has not been elucidated, we recently showed expression of inflammatory mediators, neutrophil infiltration and mucosal surface injury in the absence of bacterial infection using a human model of tracheal injury. As it has been clearly shown that neutrophil infiltration and activation can be driven in response to sterile cell death8, our preliminary data suggest that the link between Foley catheter and possible bladder neutrophil accumulation is through mucosal cell injury.
|Study Type :||Observational|
|Actual Enrollment :||58 participants|
|Official Title:||Foley Catheter Related Bladder Discomfort (FCRBD): Role of Neutrophil Cells|
|Actual Study Start Date :||November 21, 2016|
|Actual Primary Completion Date :||August 21, 2017|
|Actual Study Completion Date :||August 28, 2017|
Foley catheter group
Urine collection and blood collection and NRS for pain in patients having surgery for which their surgeon has ordered placement of a Foley catheter.
Other: urine collection
Other: Blood collection
Healthy control group
Blood collection in healthy volunteers from the Research Participant Registry or recruited from posters around the Washington University campus
Other: Blood collection
- Neutrophil surface marker changes in subjects that experience Foley catheter related bladder discomfort [FCRBD] [ Time Frame: Change from baseline [immediately after catheter placement] until catheter removal [post-operative day 1, 2, 3]. ]Changes in surface inflammatory markers on polymorphonuclear neutrophils associated with bladder injury secondary to Foley catheter placement.
Biospecimen Retention: Samples With DNA
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT03118284
|United States, Missouri|
|Washington University in St Louis|
|Saint Louis, Missouri, United States, 63110|