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...

Introduction Scientific studies have shown that hypoglycaemia is an important risk factor for adverse events in cardiac intensive care. Nursing management of blood glucose, via protocol, is an important tool to avoid cases of hypoglycaemia. Objective We evaluate the efficacy and safety of a glycemia control protocol based on nursing management in diabetic patients in Intensive Care Unit. Material and methods We conducted a retrospective analysis on 500 patients hospitalized for acute coronary syndrome or heart failure, with an average age of 75±12 years, clinically stable. The protocol used provides, on medical indication, the suspension of home therapy (both oral hypoglycemic agents and insulin) and the introduction of insulin therapy according to the scheme 0.2/0.5 IU/kg/day. The dosage lower than 0.2 IU/kg/day is used for patients in home therapy with oral hypoglycemic agents and basal blood sugar <150 mg/dl and the dose greater than 0.5 IU/kg/day for patients already on home insulin therapy and basal blood sugar> at 200 mg/dl. The intermediate dosage. 3–0.4 IU/kg/day is instead used in patients with glycaemia between 150 and 200 mg/dl regardless of home therapy. On the basis of the dosage schedule, the daily insulin requirement is obtained which is then administered at 50% as a slow analogue at 10 pm and at 50% as a rapid analogue, further divided into three doses with each main meal. Once the initial therapy has been set, the nurse acts autonomously according to a correction algorithm (based on the calculation of the correction factor (FC) according to the formula FC = 3000/body weight in kg or FC = 1700/total daily dose of insulin > FC = reduction in blood glucose in mg/dl determined by 1 IU of insulin) which provides for the modification of insulin therapy based on the patient's weight and the blood glucose values measured with sticks at 8, 12, 18 and 22. If during hospitalization and/or discharge, inadequately controlled glycemic values persist, the patient is sent to diabetes advice and the current home therapy is resumed upon discharge or according to diabetes advice. Results We observed an excellent pre and post prandial glucose control with extremely reduced incidence of hypoglycaemia which occurred in only 3 cases, one of which with severe hypoglycaemia (glucose detected <40 mg/dl, resolved with the administration of glucose 33 20ml% followed by infusion of 10% glucose solution and glycemic stick after 15') for administration error and two with moderate hypoglycaemia (glucose detected between 40–70 mg/dl resolved with the reduction of 2 IU of rapid analogue and repeated stick post prandial). Conclusions A nursing management protocol for blood glucose values in patients with diabetes mellitus hospitalized for acute coronary syndrome or heart failure is safe and allows good control of blood glucose values. Funding Acknowledgement Type of funding source: None

Resumen. Tema y alcance: este artículo pretende ofrecer al lector una mirada general sobre la toxoplasmosis, una zoonosis causada por Toxoplasma gondii que afecta tanto a los hospederos intermediarios, como a los definitivos. Buscamos que pueda entenderse la dinámica de la enfermedad, dejando de lado ciertos mitos al respecto. Características: los félidos (Felidae) son los hospederos definitivos, entre los cuales encontramos a los gatos como los más cercanos a la especie humana, que desarrollan la forma sexuada del parásito y arrojan al medio los ooquistes infectivos; de allí que su presencia es esencial en el ciclo biológico de T. gondii. Hallazgos: las investigaciones sobre gatos a nivel mundial son limitadas dado que existe una alta complejidad en la toma de muestras; sin embargo, se dispone de una amplia variedad de estudios sobre la taxonomía, la morfología, el ciclo de vida y la biología molecular, y sobre la distribución epidemiológica, sus hospederos, las vías de transmisión, las fuentes de contaminación y los factores de riesgo asociados con la infección dentro de esta especie y hacia otras vulnerables. Conclusiones: el conocimiento acerca de esta parasitosis es de gran importancia, sobre todo en los casos de mujeres embarazadas y personas inmunodeprimidas, en quienes se pueden manifestar complicaciones de la enfermedad.

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