RESUMEN
BACKGROUND: Hospital readmission occurs often and is difficult to predict. Polypharmacy has been identified as a potential risk factor for hospital readmission. However, the overall impact of the number of discharge medications on hospital readmission is still undefined. METHODS: To determine whether the number of discharge medications is predictive of thirty-day readmission using a retrospective cohort study design performed at Barnes-Jewish Hospital from January 15, 2013 to May 9, 2013. The primary outcome assessed was thirty-day hospital readmission. We also assessed potential predictors of thirty-day readmission to include the number of discharge medications. RESULTS: The final cohort had 5507 patients of which 1147 (20.8 %) were readmitted within thirty days of their hospital discharge date. The number of discharge medications was significantly greater for patients having a thirty-day readmission compared to those without a thirty-day readmission (7.2 ± 4.1 medications [7.0 medications (4.0 medications, 10.0 medications)] versus 6.0 ± 3.9 medications [6.0 medications (3.0 medications, 9.0 medications)]; P < 0.001). There was a statistically significant association between increasing numbers of discharge medications and the prevalence of thirty-day hospital readmission (P < 0.001). Multiple logistic regression identified more than six discharge medications to be independently associated with thirty-day readmission (OR, 1.26; 95 % CI, 1.17-1.36; P = 0.003). Other independent predictors of thirty-day readmission were: more than one emergency department visit in the previous six months, a minimum hemoglobin value less than or equal to 9 g/dL, presence of congestive heart failure, peripheral vascular disease, cirrhosis, and metastatic cancer. A risk score for thirty-day readmission derived from the logistic regression model had good predictive accuracy (AUROC = 0.661 [95 % CI, 0.643-0.679]). CONCLUSIONS: The number of discharge medications is associated with the prevalence of thirty-day hospital readmission. A risk score, that includes the number of discharge medications, accurately predicts patients at risk for thirty-day readmission. Our findings suggest that relatively simple and accessible parameters can identify patients at high risk for hospital readmission potentially distinguishing such individuals for interventions to minimize readmissions.
Asunto(s)
Conciliación de Medicamentos , Alta del Paciente , Readmisión del Paciente/tendencias , Adulto , Anciano , Estudios de Cohortes , Servicio de Urgencia en Hospital , Femenino , Insuficiencia Cardíaca , Humanos , Modelos Logísticos , Masculino , Persona de Mediana Edad , Modelos Teóricos , Análisis Multivariante , Polifarmacia , Factores de RiesgoRESUMEN
BACKGROUND: Episodes of patient deterioration on hospital units are expected to increasingly contribute to morbidity and healthcare costs. OBJECTIVE: To determine if real-time alerts sent to the rapid response team (RRT) improved patient care. DESIGN: Randomized, controlled trial. SETTING: Eight medicine units (Barnes-Jewish Hospital). PATIENTS: Five hundred seventy-one patients. INTERVENTION: Real-time alerts generated by a validated deterioration algorithm were sent real-time to the RRT (intervention) or hidden (control). MEASUREMENTS: Intensive care unit (ICU) transfer, hospital mortality, hospital duration. RESULTS: ICU transfer (17.8% vs 18.2%; odds ratio: 0.972; 95% confidence interval [CI]: 0.635-1.490) and hospital mortality (7.3% vs 7.7%; odds ratio: 0.947; 95% CI: 0.509-1.764) were similar for the intervention and control groups. The number of patients requiring transfer to a nursing home or long-term acute care hospital was similar for patients in the intervention and control groups (26.9% vs 26.3%; odds ratio: 1.032; 95% CI: 0.712-1.495). Hospital duration (8.4 ± 9.5 days vs 9.4 ± 11.1 days; P = 0.038) was statistically shorter for the intervention group. The number of RRT calls initiated by the primary care team was similar for the intervention and control groups (19.9% vs 16.5%; odds ratio: 1.260; 95% CI: 0.823-1.931). CONCLUSIONS: Real-time alerts sent to the RRT did not reduce ICU transfers, hospital mortality, or the need for subsequent long term care. However, hospital length of stay was modestly reduced.
Asunto(s)
Sistemas de Computación/tendencias , Mortalidad Hospitalaria/tendencias , Equipo Hospitalario de Respuesta Rápida/tendencias , Tiempo de Internación/tendencias , Sistemas de Entrada de Órdenes Médicas/tendencias , Grupo de Atención al Paciente/tendencias , Anciano , Femenino , Humanos , Masculino , Persona de Mediana EdadRESUMEN
OBJECTIVES: Amyloid-beta(42) (Abeta(42)) appears central to Alzheimer's disease (AD) pathogenesis and is a major component of amyloid plaques. Mean cerebrospinal fluid (CSF) Abeta(42) is decreased in dementia of the Alzheimer's type. This decrease may reflect plaques acting as an Abeta(42) "sink," hindering transport of soluble Abeta(42) between brain and CSF. We investigated this hypothesis. METHODS: We compared the in vivo brain amyloid load (via positron emission tomography imaging of the amyloid-binding agent, Pittsburgh Compound-B [PIB]) with CSF Abeta(42) and other measures (via enzyme-linked immunosorbent assay) in clinically characterized research subjects. RESULTS: Subjects fell into two nonoverlapping groups: those with positive PIB binding had the lowest CSF Abeta(42) level, and those with negative PIB binding had the highest CSF Abeta(42) level. No relation was observed between PIB binding and CSF Abeta(40), tau, phospho-tau(181), plasma Abeta(40), or plasma Abeta(42). Importantly, PIB binding and CSF Abeta(42) did not consistently correspond with clinical diagnosis; three cognitively normal subjects were PIB-positive with low CSF Abeta(42), suggesting the presence of amyloid in the absence of cognitive impairment (ie, preclinical AD). INTERPRETATION: These observations suggest that brain amyloid deposition results in low CSF Abeta(42), and that amyloid imaging and CSF Abeta(42) may potentially serve as antecedent biomarkers of (preclinical) AD.
Asunto(s)
Enfermedad de Alzheimer/líquido cefalorraquídeo , Péptidos beta-Amiloides/líquido cefalorraquídeo , Amiloide/metabolismo , Diagnóstico por Imagen , Fragmentos de Péptidos/líquido cefalorraquídeo , Anciano , Anciano de 80 o más Años , Enfermedad de Alzheimer/patología , Femenino , Humanos , Procesamiento de Imagen Asistido por Computador/métodos , Masculino , Memoria/fisiología , Persona de Mediana Edad , Pruebas Neuropsicológicas/estadística & datos numéricos , Distribución TisularRESUMEN
Alzheimer's disease (AD) and antecedent factors associated with AD were explored using amyloid imaging and unbiased measures of longitudinal atrophy in combination with reanalysis of previous metabolic and functional studies. In total, data from 764 participants were compared across five in vivo imaging methods. Convergence of effects was seen in posterior cortical regions, including posterior cingulate, retrosplenial, and lateral parietal cortex. These regions were active in default states in young adults and also showed amyloid deposition in older adults with AD. At early stages of AD progression, prominent atrophy and metabolic abnormalities emerged in these posterior cortical regions; atrophy in medial temporal regions was also observed. Event-related functional magnetic resonance imaging studies further revealed that these cortical regions are active during successful memory retrieval in young adults. One possibility is that lifetime cerebral metabolism associated with regionally specific default activity predisposes cortical regions to AD-related changes, including amyloid deposition, metabolic disruption, and atrophy. These cortical regions may be part of a network with the medial temporal lobe whose disruption contributes to memory impairment.
Asunto(s)
Enfermedad de Alzheimer/metabolismo , Enfermedad de Alzheimer/patología , Amiloide/metabolismo , Memoria/fisiología , Adolescente , Adulto , Anciano , Enfermedad de Alzheimer/psicología , Amiloide/fisiología , Femenino , Humanos , Estudios Longitudinales , Masculino , Tomografía de Emisión de Positrones , Lóbulo Temporal/metabolismo , Lóbulo Temporal/patologíaRESUMEN
Inhibition or deletion of cyclooxygenase (COX)-2 has been demonstrated to protect against squamous cell cancer in many studies. Although much effort has focused on COX-2 inhibition, recent work indicates that COX-1 deletion may be nearly as protective. In this study, we used SKH-1 hairless mice in which COX-1 was selectively deleted to examine the role of COX-1 in photocarcinogenesis. After UV exposure, 40-60% less prostaglandin E2 was detected in COX-1-/- animals compared with wild-type (WT) controls. A 4-fold induction of keratinocyte apoptosis was observed in knockouts relative to WT animals, as documented by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling and caspase-3 staining. Proliferation was not significantly different in COX-1+/+, COX-1+/-, and COX-1-/- animals. When susceptibility to UV-induced tumor formation was studied, tumor number, average tumor size, and time of tumor onset in COX-1-/- animals were identical to WT controls. Thus, enhanced apoptosis did not alter UV-induced skin carcinogenesis, suggesting other effects are key to nonsteroidal anti-inflammatory drug chemoprevention. These results contrast sharply with data obtained using the classic 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate cancer model in which a prominent protective effect of COX-1-/- is present. The lack of protection observed here confirms cancer mechanisms are distinct in UV- and tumor promotor-induced cancer models and indicates that chemoprevention strategies must specifically address cancer causes to be effective.