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Purpose Changes in electrolyte homeostasis are important causes of acid-base disorders. While the effects of chloride are well studied, only little is known of the potential contributions of sodium to metabolic acid-base state. Thus, we investigated the effects of intensive care unit (ICU)-acquired hypernatremia on acid-base state. Methods We included critically ill patients who developed hypernatremia, defined as a serum sodium concentration exceeding 149 mmol/L, after ICU admission in this retrospective study. Data on electrolyte and acid-base state in all included patients were gathered in order to analyze the effects of hypernatremia on metabolic acid-base state by use of the physical-chemical approach. Results A total of 51 patients were included in the study. The time of rising serum sodium and hypernatremia was accompanied by metabolic alkalosis. A transient increase in total base excess (standard base excess from 0.1 to 5.5 mmol/L) paralleled by a transient increase in the base excess due to sodium (base excess sodium from 0.7 to 4.1 mmol/L) could be observed. The other determinants of metabolic acid-base state remained stable. The increase in base excess was accompanied by a slight increase in overall pH (from 7.392 to 7.429, standard base excess from 0.1 to 5.5 mmol/L). Conclusions Hypernatremia is accompanied by metabolic alkalosis and an increase in pH. Given the high prevalence of hypernatremia, especially in critically ill patients, hypernatremic alkalosis should be part of the differential diagnosis of metabolic acid-base disorders., Author(s): Gregor Lindner [sup.1], Christoph Schwarz [sup.2], Heidelinde Grüssing [sup.3], Nikolaus Kneidinger [sup.4], Andreas Fazekas [sup.5] [sup.6], Georg-Christian Funk [sup.5] [sup.6] Author Affiliations: (1) grid.411656.1, 0000000404790855, Department of Emergency Medicine, [...]

Purpose Measuring or calculating plasma osmolality is of interest in critical care medicine. Moreover, the osmolal gap (i.e. the difference between the measured and calculated osmolality) helps in the differentiation of metabolic acidosis. A variety of formulas for calculating osmolality have been published, most of them relying on sodium, urea and glucose. A novel formula developed by Zander has recently been published, which also takes into account the effects of potassium, chloride, lactate and bicarbonate on osmolality. We evaluate the previously published formulas including the novel formula by comparing calculated and measured osmolality. Methods Arterial or venous blood samples from 41 outpatients and 195 acutely ill inpatients (total 236 subjects) were used to compare measured osmolality with calculated osmolality as obtained from 36 published formulas including the new formula. The performance of the formulas was statistically evaluated using the method of Bland and Altman. Results Mean differences up to 35 mosmol/kg H.sub.2O were observed between measured and calculated osmolality using the previously published formulas. In contrast, the novel formula had a negligible mean difference of 0.5 mosmol/kg H.sub.2O. The novel formula also had the closest 95 % limits of agreement ranging from -6.5 to 7.5 mosmol/kg H.sub.2O. Conclusion Only 4 out of the 36 evaluated formulas gave mean differences between measured and calculated osmolality of less than 1 mosmol/kg H.sub.2O. Zander's novel formula showed excellent concordance with measured osmolality and facilitates a more precise diagnosis based on blood gas analysers. The new equation has the potential to replace separate measurements of osmolality in many cases., Author(s): Andreas S. Fazekas [sup.1] [sup.2], Georg-Christian Funk [sup.1] [sup.2], Daniela S. Klobassa [sup.3], Horst Rüther [sup.3], Ingrid Ziegler [sup.3], Rolf Zander [sup.4], Hans-Jürgen Semmelrock [sup.5] Author Affiliations: (1) grid.417304.5, [...]

Summary: Tumor dissemination and recurrence is attributed to highly resistant cancer stem cells (CSCs) which may constitute a fraction of circulating tumor cells (CTCs). Small cell lung cancer (SCLC) constitutes a suitable model to investigate the relation of CTCs and CSCs due to rapid tumor spread and a high number of CTCs. Expansion of five SCLC CTC lines (BHGc7, 10, 16, 26 and UHGc5) in vitro at our institution allowed for the analysis of CSC markers and cytotoxicity of the CSC-selective drugs salinomycin and niclosamide against CTC single cell suspensions or CTC spheroids/ tumorospheres (TOS). Salinomycin exerted dose-dependent cytotoxicity against the SCLC lines but, with exception of BHGc7 TOS, there was no markedly enhanced activity against TOS. Similarly, niclosamide exhibits high activity against BHGc7 TOS and UHGc5 TOS but not against the other CTC spheroids. High expression of the CSC marker CD133 was restricted to three SCLC tumor lines and the BHGc10 CTC line. All SCLC CTCs are CD24-positive but lack expression of CD44 and ABCG2 in contrast to the SCLC tumor lines which show a phenotype more similar to that of CSCs. The stem cell marker SOX2 was found in all CTC lines and SCLC GLC14/16, whereas elevated expression of Oct-3/4 and Nanog was restricted to BHGc26 and UHGc5. In conclusion, the SCLC CTCs established from patients with relapsed disease lack a typical CSC phenotype in respect to chemosensitivity to CSC-selective drugs, surface markers, expression of pluripotent stem cell and transcription factors. [ABSTRACT FROM AUTHOR]

The epidemiology of chronic obstructive pulmonary disease (COPD) in critically ill patients is largely unknown. The aims of the study were: 1) to determine whether COPD, either as the cause of intensive care unit (ICU) admission or as a comorbid condition, is an independent risk factor for increased morbidity and mortality; and 2) to investigate time trends in proportion and outcome of acute respiratory failure in patients with COPD admitted to ICUs. Prospectively recorded data from 194 453 adults consecutively admitted to 87 Austrian ICUs over a period of 11 years (1998-2008) were retrospectively analysed. COPD was present in 8.6% of all patients. The risk-adjusted mortality of patients with COPD was higher than in patients without COPD. The presence of COPD was an independent risk factor for increased mortality and was associated with prolonged mechanical ventilation and prolonged weaning. During the course of the 11 years, the proportion of acute respiratory failure due to COPD increased by about two-thirds, and the use of noninvasive ventilation within the COPD cohort more than doubled. Simultaneously, the risk-adjusted mortality of patients with COPD improved. In critically ill patients, the presence of COPD is increasing and is an independent risk factor for mortality and morbidity.