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1.
BMJ Open Qual ; 10(1)2021 01.
Article in English | MEDLINE | ID: mdl-33526446

ABSTRACT

Delirium is a serious and common condition that leads to significant adverse health outcomes for hospitalised older adults. It occurs in 30%-55% of patients with hip fractures and is one of the most common postoperative complications in older adults undergoing orthopaedic surgery. Multicomponent, non-pharmacological interventions can reduce delirium incidence by up to 30% but are often challenging to implement as part of routine care. We identified a gap in the delivery of non-pharmacological interventions on an orthopaedic unit. This project aimed to implement a bedside sign on an orthopaedic unit to reduce the occurrence of delirium by prompting staff to use multicomponent evidence-based delirium prevention strategies for at-risk older adults. Quality improvement methods were used to integrate and optimise the use of a bedside 'delirium prevention' sign on an orthopaedic unit.The sign was implemented in four target rooms and sign completion rates increased from 47% to 83% (95% CI 71.7% to 94.9%; p<0.001) over a 10-month period. The sign did not have a significant impact on delirium prevalence. The mean Confusion Assessment Method (CAM)+ rate during the baseline period was 8% with an absolute increase in the intervention period to 11.4% (95% CI 7.2% to 15.8%; p=0.31). There were no significant shifts or trends in the run chart for the proportion of patients with CAM+ scores over time. The sign was well received by staff, who reported it was a worthwhile use of time and prompted use of non-pharmacological interventions. This quality improvement project successfully integrated a novel, low-cost, feasible and evidence-based approach into routine clinical care to support staff to deliver non-pharmacological interventions. Given the increased pressures on front-line staff in hospital, tools that reduce cognitive load at the bedside are important to consider when caring for a vulnerable older adult patient population.


Subject(s)
Delirium , Orthopedics , Aged , Delirium/epidemiology , Delirium/prevention & control , Humans , Inpatients , Quality Improvement
2.
J Alzheimers Dis ; 46(3): 553-69, 2015.
Article in English | MEDLINE | ID: mdl-25812852

ABSTRACT

The small, calcium-sensor protein, calmodulin, is ubiquitously expressed and central to cell function in all cell types. Here the literature linking calmodulin to Alzheimer's disease is reviewed. Several experimentally-verified calmodulin-binding proteins are involved in the formation of amyloid-ß plaques including amyloid-ß protein precursor, ß-secretase, presenilin-1, and ADAM10. Many others possess potential calmodulin-binding domains that remain to be verified. Three calmodulin binding proteins are associated with the formation of neurofibrillary tangles: two kinases (CaMKII, CDK5) and one protein phosphatase (PP2B or calcineurin). Many of the genes recently identified by genome wide association studies and other studies encode proteins that contain putative calmodulin-binding domains but only a couple (e.g., APOE, BIN1) have been experimentally confirmed as calmodulin binding proteins. At least two receptors involved in calcium metabolism and linked to Alzheimer's disease (mAchR; NMDAR) have also been identified as calmodulin-binding proteins. In addition to this, many proteins that are involved in other cellular events intimately associated with Alzheimer's disease including calcium channel function, cholesterol metabolism, neuroinflammation, endocytosis, cell cycle events, and apoptosis have been tentatively or experimentally verified as calmodulin binding proteins. The use of calmodulin as a potential biomarker and as a therapeutic target is discussed.


Subject(s)
Alzheimer Disease/metabolism , Calmodulin-Binding Proteins/metabolism , Calcium/metabolism , Calmodulin/metabolism , Humans , Memory Disorders/etiology , Memory Disorders/metabolism , Memory Disorders/pathology , Neurofibrillary Tangles/metabolism , Neurofibrillary Tangles/pathology , Plaque, Amyloid/metabolism , Plaque, Amyloid/pathology , Receptors, Cholinergic/metabolism
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