Background: Hyperglycemia is prevalent and is associated with an increase in morbidity and mortality in hospitalized patients. Insulin therapy is the most appropriate method for controlling glycemia in hospital, but is associated with increased risk of hypoglycemia, which is a barrier to achieving glycemic goals. Areas of Uncertainty: Optimal glycemic targets have not been established in the critical and noncritical hospitalized patients, and there are different modalities of insulin therapy. The primary purpose of this review is to discuss controversy regarding appropriate glycemic targets and summarize the evidence about the safety and efficacy of insulin therapy in critical and noncritical care settings. Data Sources: A literature search was conducted through PubMed with the following key words (inpatient hyperglycemia, inpatient diabetes, glycemic control AND critically or non-critically ill patient, Insulin therapy in hospital). Results: In critically ill patient, blood glucose levels >180 mg/dL may increase the risk of hospital complications, and blood glucose levels <110 mg/dL have been associated with an increased risk of hypoglycemia. Continuous intravenous insulin infusion is the best method for achieving glycemic targets in the critically ill patient. The ideal glucose goals for noncritically ill patients remain undefined and must be individualized according to the characteristics of the patients. A basal-bolus insulin strategy resulted in better glycemic control than sliding scale insulin and lower risk of hypoglycemia than premixed insulin regimen. Conclusions: Extremes of blood glucose lead to poor outcomes, and target glucose range of 110–180 mg/dL may be appropriate for most critically ill patients and noncritically ill patients. Insulin is the most appropriate pharmacologic agent for effectively controlling glycemia in hospital. A continuous intravenous insulin infusion and scheduled basal-bolus-correction insulin are the preferred modalities for glycemic control in critically and noncritically ill hospitalized patients, respectively.
Critical Care 2017, 21(Suppl 1):P349 Introduction Imbalance in cellular energetics has been suggested to be an important mechanism for organ failure in sepsis and septic shock. We hypothesized that such energy imbalance would either be caused by metabolic changes leading to decreased energy production or by increased energy consumption. Thus, we set out to investigate if mitochondrial dysfunction or decreased energy consumption alters cellular metabolism in muscle tissue in experimental sepsis. Methods We submitted anesthetized piglets to sepsis (n = 12) or placebo (n = 4) and monitored them for 3 hours. Plasma lactate and markers of organ failure were measured hourly, as was muscle metabolism by microdialysis. Energy consumption was intervened locally by infusing ouabain through one microdialysis catheter to block major energy expenditure of the cells, by inhibiting the major energy consuming enzyme, N+/K + -ATPase. Similarly, energy production was blocked infusing sodium cyanide (NaCN), in a different region, to block the cytochrome oxidase in muscle tissue mitochondria. Results All animals submitted to sepsis fulfilled sepsis criteria as defined in Sepsis-3, whereas no animals in the placebo group did. Muscle glucose decreased during sepsis independently of N+/K + -ATPase or cytochrome oxidase blockade. Muscle lactate did not increase during sepsis in naïve metabolism. However, during cytochrome oxidase blockade, there was an increase in muscle lactate that was further accentuated during sepsis. Muscle pyruvate did not decrease during sepsis in naïve metabolism. During cytochrome oxidase blockade, there was a decrease in muscle pyruvate, independently of sepsis. Lactate to pyruvate ratio increased during sepsis and was further accentuated during cytochrome oxidase blockade. Muscle glycerol increased during sepsis and decreased slightly without sepsis regardless of N+/K + -ATPase or cytochrome oxidase blocking. There were no significant changes in muscle glutamate or urea during sepsis in absence/presence of N+/K + -ATPase or cytochrome oxidase blockade. ConclusionsThese results indicate increased metabolism of energy substrates in muscle tissue in experimental sepsis. Our results do not indicate presence of energy depletion or mitochondrial dysfunction in muscle and should similar physiologic situation be present in other tissues, other mechanisms of organ failure must be considered. , and long-term follow up has shown increased fracture risk [2]. It is unclear if these changes are a consequence of acute critical illness, or reduced activity afterwards. Bone health assessment during critical illness is challenging, and direct bone strength measurement is not possible. We used a rodent sepsis model to test the hypothesis that critical illness causes early reduction in bone strength and changes in bone architecture. Methods 20 Sprague-Dawley rats (350 ± 15.8g) were anesthetised and randomised to receive cecal ligation and puncture (CLP) (50% cecum length, 18G needle single pass through anterior and posterior wa...
Gut microbiota can contribute to the development and progression of non-alcoholic fatty liver disease (NAFLD). In fact, some specific changes of gut microbiota are observed in patients in what is called dysbiota. There has been a lot of investigation by using a variety of interventions, including diet, showing the possibility to modify components of gastrointestinal dysbiota towards healthy and multivariate microbiota to restore physiologic status. One of the main focuses has been dietary fiber (DF), in which most of its variants are prebiotics. The highest effective treatment for NAFLD is, so far, weight loss achieved by caloric restriction. DF supplementation with oligofructose facilitates weight loss, enhances the production of beneficial metabolites, decreases some pathogenic bacteria population by increasing Bifidobacteria, and has effects on intestinal barrier permeability. DF use has been associated with improvement in diverse metabolic diseases, including NAFLD, by modifying gut microbiota. Additionally, it has been shown that a higher insoluble fiber consumption (≥7.5 g/day) revealed improvements in 3 different scores of liver fibrosis. Further research is needed, but given the evidence available, it is reasonable to prescribe its consumption in early stages of NAFLD in order to prevent disease progression.
Background And Aims Patients affected by COVID-19 may develop disease related malnutrition (DRM) due to the catabolic situation, symptoms that interfere with intake and prolonged hospital stay. This study aims to know the percentage of patients admitted for COVID-19 who required artificial nutrition (AN), their clinical characteristics, as well as the prevalence of DRM and the risk of sarcopenia at hospital discharge and after 6 months. Material And Methods Observational, prospective study, with successive inclusion of adult patients admitted for COVID-19 in whom institutional nutritional support (NS) care protocol was applied. Those who received AN underwent a nutritional screening by Short Nutritional Assessment Questionnaire (SNAQ) and an assessment by Subjective Global Assessment (SGA) at hospital discharge, as well as a screening for sarcopenia (SARC-F test) and SNAQ re-test 15 days and 6 months after by a phone call. Symptoms related to food intake, anthropometric and analytical data were also collected. Results We evaluated 936 patients with a mean age of 63.7 ± 15.3 years; predominantly male (59.7%), overweight 41%, obesity 40.4%; hypertension 52.9%; diabetes mellitus 26.6% and cancer 10.4%. The stay hospital length was 17.3 ± 13.8 days and 13.6% patients died during hospitalization. The modality of nutritional support was: 86.1% dietary adaptation + oral nutritional supplements (ONS); 12.4% enteral nutrition (EN) by nasogastric (NG) tube; 0.9% parenteral nutrition (PN) and 0.6% EN plus PN. Focusing on patients who received AN, follow-up post discharge was possible in 62 out of 87 who survived. Of these, at the time of hospital discharge, 96.7% presented nutritional risk by SNAQ and 100% malnutrition by SGA (20% B; 80% C). During admission, 82.3% presented intense anorexia and the mean weight loss was 10.9 ± 6 Kg (p <0.001). Fifteen days after being discharged, 12.9% still had anorexia, while hyperphagia appeared in 85.5% of the patients and risk of sarcopenia by SARC-F was present in 87.1% of them. Six months after discharge, 6.8% still had anorexia and 3.4% hyperphagia, with a global weight gain of 4.03± 6.2 Kg (p=<0.0001). Risk of malnutrition was present in only 1.7% of the patients, although risk of sarcopenia persisted in 49.2%. Conclusion All patients admitted by COVID-19 for whom EN or PN were indicated following an institutional protocol still presented malnutrition at hospital discharge, and almost all showed risk of sarcopenia, that persisted in almost half of them at 6 months. These findings suggest that nutritional and functional problems persist in these patients after discharge, indicating that they require prolonged nutritional support and monitoring.
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