RESUMO
BACKGROUND: Home return after critical care is very important not only to patients and families. To move back home, patients have to fulfill two conditions: survive, and have a relatively good functional status. In addition, home return could be considered a low-cost outcome because of the reduced permanent healthcare costs. METHODS: To determine the factors influencing the home-return probability of critically ill elderly patients 6 months after an intensive care unit (ICU) admission, we analyzed a cohort of patients aged 65 years or older admitted to an ICU. Demographic and social parameters, as well as admission diagnosis, underlying diseases, severity scores, ICU stay parameters, and complications were recorded. The final outcome was the place of stay (or death) 180 days after ICU admission. RESULTS: Of 526 patients, 72% of the cohort and 93% of hospital survivors were able to return to their homes. Among the variables used in the multivariate logistic regression, advanced age, length of hospital stay before ICU admission, severity of acute illness, diagnosis category, and complications, as well as certain comorbidities, such as chronic heart failure or a neoplasia, were independently negatively associated with a home return. CONCLUSION: Some interesting factors were identified in this single-center study. They could be considered for a multicenter study to build a universal prediction model for home return. Home return could be used for elderly patients as a surrogate for outcomes that are very important to the elderly but also to health politics.
Assuntos
Cuidados Críticos/estatística & dados numéricos , Unidades de Terapia Intensiva/estatística & dados numéricos , Idoso , Idoso de 80 Anos ou mais , Comorbidade , Coleta de Dados , Interpretação Estatística de Dados , Feminino , Seguimentos , Custos de Cuidados de Saúde , Hospitalização/estatística & dados numéricos , Humanos , Tempo de Internação , Modelos Logísticos , Masculino , Alta do Paciente , Estudos Prospectivos , Respiração Artificial , Fatores de Risco , Tamanho da Amostra , Resultado do TratamentoRESUMO
Secondary to severe hospital outbreaks due to hypervirulent strains of Clostridium difficile, several surveillance systems in North-America and Europe observed an increase in infections due to this micro-organism, also in the outpatient setting. The case reported in the present article illustrates the fulminant presentation that a C. difficile colitis can show in a previously healthy person without prior contact with healthcare facilities. It introduces a review of some recent publications on the current changes in the epidemiology, clinical presentation, diagnosis and treatment of this disease.
Assuntos
Clostridioides difficile , Enterocolite Pseudomembranosa/epidemiologia , Antibacterianos/uso terapêutico , Infecções Comunitárias Adquiridas/diagnóstico , Infecções Comunitárias Adquiridas/tratamento farmacológico , Infecções Comunitárias Adquiridas/epidemiologia , Resistência Microbiana a Medicamentos , Enterocolite Pseudomembranosa/diagnóstico , Enterocolite Pseudomembranosa/tratamento farmacológico , Feminino , Humanos , Pessoa de Meia-IdadeAssuntos
Infarto Cerebral/diagnóstico , Infarto Cerebral/patologia , Eletroencefalografia , Sono/fisiologia , Tálamo/patologia , Idoso , Alcoolismo/complicações , Contagem de Células Sanguíneas , Encéfalo/patologia , Coma/etiologia , Humanos , Testes de Função Hepática , Imageamento por Ressonância Magnética , Masculino , Acidente Vascular Cerebral/etiologia , Acidente Vascular Cerebral/terapiaRESUMO
Skeletal muscle CoA and carnitine metabolism were investigated in six human volunteers at rest and after exhaustive exercise under normoxic and hypoxic conditions. In comparison to the values at rest, exhaustive exercise was associated with a three- to fourfold increase in the skeletal muscle lactate, and with a twofold increase in the acetyl-CoA content, both under normoxic and hypoxic conditions. Since exercise did not significantly affect the skeletal muscle CoA radical (CoASH), total acid-soluble, or total CoA contents, the increase in the acetyl-CoA content was at the expense of short-chain acyl-CoAs different from acetyl-CoA. With exhaustive exercise, the skeletal muscle acetylcarnitine and short-chain acylcarnitine contents increased by a factor of three to four both under normoxic and hypoxic conditions. In contrast to the CoA pool, these increases were associated with a decrease in the free carnitine content, whereas the total acid-soluble and total carnitine contents were not affected by exercise. After exhaustive exercise, the skeletal muscle acetyl-CoA/CoASH ratio showed a linear correlation with the corresponding acetylcarnitine/free carnitine ratio. The plasma short-chain acylcarnitine concentration increased by a factor of two to three during exercise, and was not significantly different from the values at rest 40 min after completion of exercise. Thus, the current studies illustrate the close interaction between the CoA and carnitine pools in the exercising human skeletal muscle, and they underscore the important role of carnitine in maintaining the muscular CoASH content during exhaustive exercise.
Assuntos
Carnitina/metabolismo , Coenzima A/metabolismo , Músculo Esquelético/metabolismo , Oxigênio/fisiologia , Esforço Físico/fisiologia , Acetilcoenzima A/metabolismo , Adulto , Hemodinâmica , Humanos , Lactatos/metabolismo , Ácido Láctico , Masculino , Músculo Esquelético/fisiologiaRESUMO
Hyperammonemia is a major contributing factor to the neurological abnormalities observed in hepatic encephalopathy and in congenital defects of ammonia detoxication. In rats variable changes in labile energy rich phosphates in the brain have been observed in hyperammonemia using biochemical methods. Using 31P-NMR spectroscopy however no significant changes of the relative concentrations of the energy rich phosphates alpha, beta and gamma-ATP, phosphocreatine, inorganic phosphate and the pH were found in the fronto parietal cortex of the urease treated hyperammonemic rat. Alterations in the metabolites of these compounds do not appear to be a major pathomechanism of ammonia toxicity in this brain area.