Background The effect of premorbid β-blocker exposure on clinical outcomes in patients with sepsis is not well characterized. We aimed to examine the association between premorbid β-blocker exposure and mortality in sepsis. Methods EMBase, MEDLINE, and Cochrane databases were searched for all studies of premorbid β-blocker and sepsis. The search was last updated on 22 June 2019. Two reviewers independently assessed, selected, and abstracted data from studies reporting chronic β-blocker use prior to sepsis and mortality. Main data extracted were premorbid β-blocker exposure, mortality, study design, and patient data. Two reviewers independently assessed the risk of bias and quality of evidence. Results In total, nine studies comprising 56,414 patients with sepsis including 6576 patients with premorbid exposure to β-blockers were eligible. For the primary outcome of mortality, two retrospective studies reported adjusted odds ratios showing a reduction in mortality with premorbid β-blocker exposure. One study showed that premorbid β-blocker exposure decreases mortality in patients with septic shock. Another study showed that continued β-blockade during sepsis is associated with decreased mortality. Conclusion This systematic review suggests that β-blocker exposure prior to sepsis is associated with reduced mortality. There was insufficient data to conduct a bona fide meta-analysis. Whether the apparent reduction in mortality may be attributed to the mitigation of catecholamine excess is unclear. Trial registration PROSPERO, CRD42019130558 registered June 12, 2019. Electronic supplementary material The online version of this article (10.1186/s13054-019-2562-y) contains supplementary material, which is available to authorized users.

OBJECTIVES: To examine the effect of premorbid β-blocker exposure on mortality and organ dysfunction in sepsis. DESIGN: Retrospective observational study. SETTING: ICUs in Australia, the Czech Republic, and the United States. PATIENTS: Total of 4,086 critical care patients above 18 years old with sepsis between January 2014 and December 2018. INTERVENTION: Premorbid beta-blocker exposure. MEASUREMENTS AND MAIN RESULTS: One thousand five hundred fifty-six patients (38%) with premorbid β-blocker exposure were identified. Overall ICU mortality rate was 15.1%. In adjusted models, premorbid β-blocker exposure was associated with decreased ICU (adjusted odds ratio, 0.80; 95% CI, 0.66–0.97; p = 0.025) and hospital (adjusted odds ratio, 0.83; 95% CI, 0.71–0.99; p = 0.033) mortality. The risk reduction in ICU mortality of 16% was significant (hazard ratio, 0.84, 95% CI, 0.71–0.99; p = 0.037). In particular, exposure to noncardioselective β-blocker before septic episode was associated with decreased mortality. Sequential Organ Failure Assessment score analysis showed that premorbid β-blocker exposure had potential benefits in reducing respiratory and neurologic dysfunction. CONCLUSIONS: This study suggests that β-blocker exposure prior to sepsis, especially to noncardioselective β blockers, may be associated with better outcome. The findings suggest prospective evaluation of β-blocker use in the management of sepsis.

Background. This retrospective study examines the relationship between admission Blood Urea Nitrogen (BUN) levels and clinical outcomes in patients with sepsis from two separate cohorts in the Czech Republic and the United States. Methods. The study included 9126 patients with sepsis between January 2014 and December 2018. Kaplan-Meier survival curves and Cox regression were used to analyse the data. An optimal cut-off was calculated by means of the Youden-Index.Results. BUN at ICU admission was categorized as 10-20, 20-40 and >40 mg/dL. Comparing the group with the highest BUN levels to the one with lowest levels, we found HR for 28 days mortality 2.764 (CI 95% 2.37-3.20; P<0.001). We derived an optimal cut-off for prediction of 28 days mortality of 23 mg/dL. The association between BUN and 28 days mortality remained significant after adjusting for potential confounders -for APACHE IV (

In the publication of this article [1], there was an error in the cited reference 23 [2] within the Family Name. This has now been updated in the original article.

Stručná historie tekutinové léčbyPočátky tekutinové léčby se vztahují k 19. století. Největším impulzem pro rozvoj nitrožilní léčby tekutinami bylo období epidemie cholery. Thomas Latta prvně popsal v Lancetu v roce 1832 použití solného roztoku v léčbě pacientů trpících cholerou. V roce 1880 Sydney Ringer pozoroval odlišné fyziologické účinky roztoků různého složení elektrolytů na žabí srdce. O 58 let později americký pediatr Alexis Hartmann přidal do původního Ringerova roztoku laktát s cílem zmírnit jeho acidifikující důsledky a vznikl roztok známý jako laktátový Ringerův roztok nebo také jako Hartmannův roztok. Z obavy před důsledky podávání velkého množství laktátu byl posléze laktát nahrazen acetátem a vznikl tzv. Ringer's acetate roztok. Konečně na konci 80. let 20. století byl registrován roztok Plasma-lyte, jehož biochemické složení se mělo co nejvíce přiblížit složení lidské plazmy. Rozvoj technologií umožňujících frakcionaci plné krve v roce 1941 umožnil první použití roztoku lidského albuminu k tekutinové resuscitaci raněných při útoku na Pearl Harbor. Omezená dostupnost a vysoká cena albuminu podnítila rozvoj dnes již nepoužívaných dextranů a zejména nové skupiny tzv. semisyntetických koloidůroztoků na bázi hydroxyetylškrobu nebo želatiny. Terminologie tekutinové terapiePři preskripci tekutinové léčby je v první řadě nutné pojmenovat základní cíl, kterého intravenózními roztoky chceme dosáhnout. Existují 4 hlavní indikace, které určují vlastní strategii tekutinové léčby.