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Anticholinergic Activity in Cerebrospinal Fluid and Serum in Individuals with Hip Fracture with and without Delirium
Author(s) -
Watne Leiv Otto,
Hall Roanna J.,
Molden Espen,
Ræder Johan,
Frihagen Frede,
MacLullich Alasdair M. J.,
Juliebø Vibeke,
Nyman Armika,
Meagher David,
Wyller Torgeir B.
Publication year - 2014
Publication title -
journal of the american geriatrics society
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.992
H-Index - 232
eISSN - 1532-5415
pISSN - 0002-8614
DOI - 10.1111/jgs.12612
Subject(s) - delirium , medicine , anticholinergic , hip fracture , cerebrospinal fluid , prospective cohort study , anesthesia , anticholinergic agents , cohort , cohort study , gastroenterology , osteoporosis , psychiatry
Objectives To examine whether anticholinergic activity ( AA ) in cerebrospinal fluid ( CSF ) and serum is associated with risk of delirium in individuals with hip fracture. Design Prospective cohort study. Setting Two university hospitals in O slo, N orway, and E dinburgh, UK . Participants Individuals admitted with acute hip fracture (N = 151). Measurements Participants were assessed daily for delirium using the C onfusion A ssessment M ethod (preoperatively and postoperative days 1–5 (all) or until discharge (participants with delirium)). Prefracture cognitive function was assessed using the I nformant Q uestionnaire on C ognitive D ecline in the E lderly ( IQCODE ). Serum was collected preoperatively and CSF at the onset of spinal anesthesia. AA in serum ( SAA ) and CSF samples was determined according to a muscarinic radio receptor bioassay. The association between AA measures and delirium was evaluated using logistic multivariate analyses. Results Fifty‐two (54%) of the participants in O slo and 20 (39%) in E dinburgh developed delirium. There was no statistically significant difference in AA between participants with and without delirium in O slo (serum: 7.02 vs 6.08 pmol/mL, P  = .54; CSF : 0.39 vs 0.48 pmol/mL, P  = .26) or in E dinburgh (serum: 1.35 vs 1.62 pmol/mL, P  = .76; CSF : 0.36 vs 0.31 pmol/mL, P  = .93). Nor was there any difference in SAA ( O slo, P  = .74; E dinburgh, P  = .51) or CSF AA ( O slo, P  = .21; E dinburgh, P  = .93) when participants were subdivided into prevalent, incident, subsyndromal, and never delirium. Stratifying participants according to prefracture cognitive status ( IQCODE ) gave the same results. Conclusion This is the first study of AA in CSF of individuals with and without delirium. The study does not support the hypothesis that central ( CSF ) or peripheral (serum) AA is an important mechanism of delirium in individuals with hip fracture.

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