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...
Aim: Medical Device-Related Pressure Ulcers are skin breakdowns related to certain medical devices that increase morbidity, lengthen hospital stays, and increase the cost of treatment. Approximately one third of reported pressure ulcers are associated with medical devices. The aim of this study is to examine the impact of a suggested nursing intervention protocol on the occurrence of medical device-related pressure ulcers in critically ill patients. Design: A prospective, quasi-experimental research design was used in this study. Methods: 100 patients participated in our study, divided into study and control groups. The researchers selected Endo-tracheal and Nasogastric tubes to examine their association with the development of pressure ulcers. The researchers observed the prevalence of pressure ulcers caused by the selected devices through daily clinical observation. Patients receiving routine care were used as a control group, while the suggested nursing intervention protocol was implemented to the study group of patients. The results of the given protocol on the study subjects were compared to the collected base line data for the control group. Results: The study revealed a highly statistically and clinically significant difference between the study and control groups in relation to incidence of endo-tracheal and nasogastric tube pressure ulcers. The results indicate that the incidence of endo-tracheal tube pressure ulcers decreased from 90% to 32.1% after implementation of the suggested nursing intervention protocol (p = 0.031), whereas the incidence of nasogastric tubes pressure ulcers fell from 77.8% to 13.1% (p = 0.012). Conclusion: the examined evidence based suggested nursing intervention protocol proved highly effective in reducing the occurrence of selected Medical Device-Related Pressure Ulcers in critically ill patients.
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