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Impact and recognition of cognitive impairment among hospitalized elders.

ABSTRACT: Older adults are predisposed to developing cognitive deficits. This increases their vulnerability for adverse health outcomes when hospitalized.To determine the prevalence and impact of cognitive impairment (CI) among hospitalized elders based on recognition by lCD-coding versus screening done on admission.Observational cohort study.Urban public hospital in Indianapolis.997 patients age 65 and older admitted to medical services between July 2006 and March 2008.Impact of CI in terms of length of stay, survival, quality of care and prescribing practices. Cognition was assessed by the Short Portable Mental Status Questionnaire (SPMSQ).424 patients (43%) were cognitively impaired. Of those 424 patients with CI, 61% had not been recognized by ICD-9 coding. Those unrecognized were younger (mean age 76.1 vs. 79.1, P <0.001); had more comorbidity (mean Charlson index of 2.3 vs.1.9, P = 0.03), had less cognitive deficit (mean SPMSQ 6.3 vs. 3.4, P < 0.001). Among elders with CI, 163 (38%) had at least one day of delirium during their hospital course. Patients with delirium stayed longer in the hospital (9.2 days vs. 5.9, P < 0.001); were more likely to be discharged into institutional settings (75% vs. 31%, P < 0.001) and more likely to receive tethers during their care (89% vs. 69%, P < 0.001), and had higher mortality (9% vs. 4%, P = 0.09).Cognitive impairment, while common in hospitalized elders, is under-recognized, impacts care, and increases risk for adverse health outcomes.

SUBMITTER: Boustani M

PROVIDER: S-EPMC2814975 | biostudies-other | 2010 Feb

REPOSITORIES: biostudies-other

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Impact and recognition of cognitive impairment among hospitalized elders.

Boustani Malaz M Baker Mary Shearer MS Campbell Noll N Munger Stephanie S Hui Siu L SL Castelluccio Pete P Farber Mark M Guzman Oscar O Ademuyiwa Adetayo A Miller David D Callahan Chris C

Journal of hospital medicine 20100201 2

<h4>Background</h4>Older adults are predisposed to developing cognitive deficits. This increases their vulnerability for adverse health outcomes when hospitalized.<h4>Objective</h4>To determine the prevalence and impact of cognitive impairment (CI) among hospitalized elders based on recognition by lCD-coding versus screening done on admission.<h4>Design</h4>Observational cohort study.<h4>Setting</h4>Urban public hospital in Indianapolis.<h4>Patients</h4>997 patients age 65 and older admitted to ...[more]

PMID: 20104623

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Project description:To evaluate whether race influences agreement between screening results and documentation of cognitive impairment and delirium.Secondary data analysis.An urban, public hospital and healthcare system.Hospitalized older adults aged 65 and older admitted to general inpatient medical services evaluated for cognitive impairment (n = 851) and evaluated for delirium (n = 424).Cognitive impairment and delirium were measured in each participant using the Short Portable Mental Status Questionnaire (SPMSQ) and the Confusion Assessment Method (CAM), respectively, as the reference identification method. Clinical documentation of cognitive impairment and delirium was defined according to the presence of International Classification of Diseases, Ninth Revision (ICD-9), codes from within 1 year before hospitalization through discharge for cognitive impairment or from hospital admission through discharge for delirium.Two hundred ninety-four participants (34%) had cognitive impairment based on SPMSQ performance, and 163 (38%) had delirium based on CAM results. One hundred seventy-one (20%) of those with cognitive impairment had an ICD-9 code for cognitive impairment, whereas 92 (22%) of those with delirium had an ICD-9 code for delirium. After considering age, sex, education, socioeconomic status, chronic comorbidity, and severity of acute illness, of those who screened positive on the SPMSQ, African Americans had a higher adjusted odds ratio (AOR) than non-African Americans for clinical documentation of cognitive impairment (AOR = 1.66, 95% confidence interval (CI) = 0.95-2.89), and of those who screened negative on the SPMSQ, African Americans had higher odds of clinical documentation of cognitive impairment (AOR = 2.10, 95% CI = 1.17-3.78) than non-African Americans. There were no differences in clinical documentation rates of delirium between African Americans and non-African Americans.Racial differences in coding for cognitive impairment may exist, resulting in higher documentation of cognitive impairment in African Americans screening positive or negative for cognitive impairment.

Project description:ObjectiveTo determine whether variants in the estrogen receptors 1 (alpha) and 2 (beta) (ESR1 and ESR2) genes are associated with cognitive impairment in non-demented elderly men and women.BackgroundSeveral single nucleotide polymorphisms (SNPs) on ESR1 and ESR2 genes have been associated with a range of hormone sensitive diseases such as breast cancer and osteoporosis. Genetic variations in ESR may also influence cognitive aging but are less studied, especially among men.MethodsWe studied 2527 participants enrolled in an ongoing prospective study of community-dwelling elders. Four SNPs from ESR1 and four from ESR2 were analyzed. We measured cognitive function with the Modified Mini-Mental Status Examination (3MS) at baseline and biannually; cognitive impairment was defined as a decline of five or more points over 4 years. We calculated odds of developing cognitive impairment across SNPs using gender-stratified logistic regression and adjusted analyses for age, education, baseline 3MS score and in addition for race.ResultsOne thousand three hundred and forty-three women (mean age 73.4) and 1184 men (mean age 73.7) comprised our cohort. Among women, after multivariate adjustment, two of the ESR1 SNPs (rs8179176, rs9340799) and two of the ESR2 SNPs (rs1256065, rs1256030) were associated with likelihood of developing cognitive impairment, although the association for rs8179176 was of trend level significance. In men, one of the ESR1 SNPs (rs728524) and two of the ESR2 (rs1255998, rs1256030) were associated with cognitive impairment. Further adjustment for race attenuated the results somewhat. There was no association between any ESR SNP and level of bioavailable estradiol but testosterone level did vary among two of the SNPs (p<0.05).ConclusionWe found that among non-demented community elders, several SNPs in the ESR1 and ESR2 genes were associated with risk of developing cognitive impairment. These findings suggest that estrogen receptor genetic variants may play a role in cognitive aging.

Project description:BackgroundThe presence of cognitive impairment (CI) among hospitalized older adults (aged 85 years and older) could interfere with the identification and treatment of other important symptoms experienced by these patients. Little is known, however, about the nursing care provided to this group. Contrasting the nursing care provided to patients with and without CI may reveal important insights about symptom treatment in the CI population.ObjectiveThe aim of this study was to examine the relationship of CI to nursing care provided and length of stay for hospitalized older adults using standardized nursing data retrieved from electronic health records.MethodsWe conducted a comparative secondary data analysis. A data set of standardized nursing plan of care data retrieved from electronic health record data of nine units at four hospitals was analyzed. The plan of care data for this study were previously transformed into one of eight categories (family, well-being, mental comfort, physical comfort, mental, safety, functional, and physiological care). Fisher exact tests were used to compare the differences in the nursing care for hospitalized older adults with and without CI. Mixed-effects models were used to examine associations of patient's cognitive status and nursing care, and cognitive status and length of stay.ResultsWe identified 4,354 unique patients; 746 (17%) had CI. We observed that older adults with CI were less likely to receive physical comfort care than those without CI for seven of nine units. Older adults' cognitive status was associated with the delivery of mental comfort care. In addition, a worsening in cognitive status was associated with an increase in length of stay for older adults with CI.DiscussionOlder adults with CI appeared to be undertreated for symptoms of pain when compared to those without CI across units. There is a need for further research to improve symptom recognition and management for this population. The presence of CI was associated with variation in nursing care provided and length of stay. Future studies that include the analysis of nursing data merged with elements stored in the electronic health record representing the contributions of other health professions are expected to provide additional insights into this gap.

Project description:Although immediate early genes (IEGs) such as Bdnf, Arc and Egr1, have been implicated in plasticity, the larger pathways related to memory and memory disorders are not well understood. Here, we combined statistical Affymetrix microarray and behavioral analyses to identify key genes and pathways associated with aging-related cognitive impairment. Aged rats were separated into cognitively unimpaired (AU) or impaired (AI) groups, based on their Morris water maze performance relative to young-adult (Y) animals. Hippocampal gene expression was assessed in Y, AU and AI on the fifth (last) day of maze training or 21 days posttraining, and in non-trained aged and young animals (eight groups, overall n = 78, one chip/animal). ANOVA, linear contrasts, and overrepresentation analyses identified genes and pathways that differed from Y generally with aging (in both AU and AI) or selectively with cognitive status (only in AI or AU). Plasticity pathways, including insulin/cAMP/IEG signaling, and glycogenolytic and lipogenic pathways, were selectively downregulated (5 days) in AI, whereas Notch2 (regulating oligodendrocyte differentiation) and myelination pathways were upregulated (particularly at 21 days). Downregulation with general aging occurred in signal transduction and axonal growth/transport pathways, whereas upegulation occurred in immune/inflammatory, lipid metabolism/transport (e.g., Lxr-Srebf1), and lysosomal pathways. In AU, receptor/signal transduction genes were selectively upregulated, suggesting possible compensatory mechanisms. Immunohistochemistry confirmed and extended results to the protein level. Thus, this study identified novel cognition-linked processes, suggesting a new model in which energy-intensive, plasticity/lipogenic processes and energy-generating pathways necessary for learning are coordinately downregulated during training, while myelinogenic programs that impair cognition are concurrently activated. Keywords: Immediate Early Genes, Insulin Signaling, Cholesterol, Myelination, Glia, Inflammation, Young and Old comparaison, behavioral-characterization, Aging-related cognitive impairment.

Project description:BackgroundCerebrospinal fluid (CSF) ?-synuclein is reduced in synucleinopathies, including dementia with Lewy bodies, and some studies have found increased CSF ?-synuclein in Alzheimer's disease (AD). No study has explored effects of CSF ?-synuclein on brain atrophy. Here we tested if baseline CSF ?-synuclein affects brain atrophy rates and if these effects vary across brain regions, and across the cognitive spectrum from healthy elders (NL), to patients with mild cognitive impairment (MCI) and AD.MethodsBaseline CSF ?-synuclein measurements and longitudinal structural brain magnetic resonance imaging was performed in 74 NL, 118 MCI patients and 55 AD patients. Effects of baseline CSF ?-synuclein on regional atrophy rates were tested in 1) four pre-hoc defined regions possibly associated with Lewy body and/or AD pathology (amygdala, caudate, hippocampus, brainstem), and 2) all available regions of interest. Differences across diagnoses were tested by assessing the interaction of CSF ?-synuclein and diagnosis (testing NL versus MCI, and NL versus AD).ResultsThe effects of CSF ?-synuclein on longitudinal atrophy rates were not significant after correction for multiple comparisons. There were tendencies for effects in AD in caudate (higher atrophy rates in subjects with higher CSF ?-synuclein, P=0.046) and brainstem (higher atrophy rates in subjects with lower CSF ?-synuclein, P=0.063). CSF ?-synuclein had significantly different effects on atrophy rates in NL and AD in brainstem (P=0.037) and caudate (P=0.006).DiscussionWith the possible exception of caudate and brainstem, the overall weak effects of CSF ?-synuclein on atrophy rates in NL, MCI and AD argues against CSF ?-synuclein as a biomarker related to longitudinal brain atrophy in these diagnostic groups. Any effects of CSF ?-synuclein may be attenuated by possible simultaneous occurrence of AD-related neuronal injury and concomitant Lewy body pathology, which may elevate and reduce CSF ?-synuclein levels, respectively.

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Impact and recognition of cognitive impairment among hospitalized elders.

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Impact and recognition of cognitive impairment among hospitalized elders.

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