Patients with sepsis syndrome commonly have low serum selenium levels. Several randomized controlled trials have examined the efficacy of selenium supplementation on mortality in patients with sepsis. To determine the efficacy and safety of high-dose selenium supplementation compared to placebo for the reduction of mortality in patients with sepsis. We searched Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, SciFinder, and Clinicaltrials.gov. Randomized controlled parallel group trials comparing selenium supplementation in doses greater than daily requirement to placebo on the outcome of mortality in patients with sepsis syndrome. Two reviewers independently applied eligibility criteria, assessed quality, and extracted data. The primary outcome was mortality; secondary outcomes were ICU length of stay, nosocomial pneumonia, and adverse events. Trial authors were contacted for additional or clarifying information. Nine trials enrolling a total of 792 patients were included. Selenium supplementation in comparison to placebo was associated with lower mortality (odds ratio, 0.73; 95% CI, 0.54, 0.98; p = 0.03; I = 0%). Among patients receiving and not receiving selenium, there was no difference in ICU length of stay (mean difference, 2.03; 95% CI, -0.51, 4.56; p = 0.12; I = 0%) or nosocomial pneumonia (odds ratio, 0.83; 95% CI, 0.28, 2.49; p = 0.74; I = 56%). Significant heterogeneity among trials in adverse event reporting precluded pooling of results. In patients with sepsis, selenium supplementation at doses higher than daily requirement may reduce mortality. We observed no impact of selenium on ICU length of stay or risk of nosocomial pneumonia.

Among the multiple causes of weaning failure from mechanical ventilation, cardiovascular dysfunction is increasingly recognized as a quite frequent cause that can be treated successfully. In this review, we summarize the contemporary evidence of the most important clinical and diagnostic aspects of weaning failure of cardiovascular origin with special focus on treatment. Pathophysiological mechanisms are complex and mainly include increase in right and left ventricular preload and afterload and potentially induce myocardial ischemia. Patients at risk include those with preexisting cardiopulmonary disease either known or suspected. Clinically, cardiovascular etiology as a predominant cause or a contributor to weaning failure, though critical for early diagnosis and intervention, may be difficult to be recognized and distinguished from noncardiac causes suggesting the need of high suspicion. A cardiovascular diagnostic workup including bedside echocardiography, lung ultrasound, electrocardiogram and biomarkers of cardiovascular dysfunction or other adjunct techniques and, in selected cases, right heart catheterization and/or coronary angiography, should be obtained to confirm the diagnosis. Official clinical practice guidelines that address treatment of a confirmed weaning-induced cardiovascular dysfunction do not exist. As the etiologies of weaning-induced cardiovascular dysfunction are diverse, principles of management depend on the individual pathophysiological mechanisms, including preload optimization by fluid removal, guided by B-type natriuretic peptide measurement, nitrates administration in excessive afterload and/or myocardial ischemia, contractility improvement in severe systolic dysfunction as well as other rational treatment in specific indications in order to lead to successful weaning from mechanical ventilation.

The objectives of this study were to investigate the incidence of candidemia, as well as the factors associated with Candida species distribution and fluconazole resistance, among patients admitted to the intensive care unit (ICU) during the COVID-19 pandemic, as compared to two pre-pandemic periods. All patients admitted to the ICU due to COVID-19 from March 2020 to October 2021, as well as during two pre-pandemic periods (2005–2008 and 2012–2015), who developed candidemia, were included. During the COVID-19 study period, the incidence of candidemia was 10.2%, significantly higher compared with 3.2% and 4.2% in the two pre-pandemic periods, respectively. The proportion of non-albicans Candida species increased (from 60.6% to 62.3% and 75.8%, respectively), with a predominance of C. parapsilosis. A marked increase in fluconazole resistance (from 31% to 37.7% and 48.4%, respectively) was also observed. Regarding the total patient population with candidemia (n = 205), fluconazole resistance was independently associated with ICU length of stay (LOS) before candidemia (OR 1.03; CI: 1.01–1.06, p = 0.003), whereas the presence of shock at candidemia onset was associated with C. albicans (OR 6.89; CI: 2.2–25, p = 0.001), and with fluconazole-susceptible species (OR 0.23; CI: 0.07–0.64, p = 0.006). In conclusion, substantial increases in the incidence of candidemia, in non-albicansCandida species, and in fluconazole resistance were found in patients admitted to the ICU due to COVID-19, compared to pre-pandemic periods. At candidemia onset, prolonged ICU LOS was associated with fluconazole-resistant and the presence of shock with fluconazole-susceptible species.

Acute kidney injury is one of the most frequent problems occurring in the critically ill patients of the intensive care units and it is well established that it increases both morbidity and mortality in these patients. Moreover, despite technological and pharmaceutical advances during the last decades, the incidence as well as the mortality associated with acute kidney injury in these patients remains unchanged. Creatinine, the most common renal dysfunction biomarker in use, has many disadvantages, such as time delay in its increase and the influence by other factors on its serum concentration, such as age, gender, muscle mass, etc. Hence, the need for better renal biomarkers in order to timely intervene for acute kidney injury prevention is imperative. The lack of an early biomarker is an obstacle for the development of new acute kidney injury prevention strategies. With the incidence of acute kidney injury reaching epidemic dimensions, the need for novel markers is urgent. During the last years, the research for finding such biomarkers has been intense. The purpose of the present article is to review the studies which have tested the predictive ability of those markers (in urine and/or plasma) for early detection of acute kidney injury in the mixed adult intensive care unit population and underline the potential limitations encountered in the various studies.

Calcitonin gene-related peptide (CGRP) is one of the most potent microvascular vasodilators identified to date. Vascular relaxation and vasodilation is mediated via activation of the CGRP receptor. This atypical receptor is made up of a G protein-coupled receptor called calcitonin receptor-like receptor (CLR), a single transmembrane protein called receptor activity-modifying protein (RAMP), and an additional protein that is required for Ga_s coupling, known as receptor component protein (RCP). Several mechanisms involved in CGRP-mediated relaxation have been identified. These include nitric oxide (NO)-dependent endothelium-dependent mechanisms or cAMP-mediated endothelium-independent pathways; the latter being more common. Subarachnoid hemorrhage (SAH) is associated with cerebral vasoconstriction that occurs several days after the hemorrhage and is often fatal. The vasospasm occurs in 30–40% of patients and is the major cause of death from this condition. The vasoconstriction is associated with a decrease in CGRP levels in nerves and an increase in CGRP levels in draining blood, suggesting that CGRP is released from nerves to oppose the vasoconstriction. This evidence has led to the concept that exogenous CGRP may be beneficial in a condition that has proven hard to treat. The present article reviews: (a) the pathophysiology of delayed ischemic neurologic deficit after SAH (b) the basics of the CGRP receptor structure, signal transduction, and vasodilatation mechanisms and (c) the studies that have been conducted so far using CGRP in both animals and humans with SAH.

Aquaporins (AQPs) are membrane proteins facilitating water and other small solutes to be transported across cell membranes. They are crucial in maintaining cellular homeostasis by regulating water permeability in various tissues. Moreover, they regulate cell migration, signaling pathways, inflammation, tumor growth, and metastasis. In critically ill patients, such as trauma, sepsis, and patients with acute respiratory distress syndrome (ARDS), which are frequently encountered in intensive care units (ICUs), water transport regulation is crucial for maintaining homeostasis, as dysregulation can lead to edema or dehydration, with the latter also implicating hemodynamic compromise. Indeed, AQPs are involved in fluid transport in various organs, including the lungs, kidneys, and brain, where their dysfunction can exacerbate conditions like ARDS, acute kidney injury (AKI), or cerebral edema. In this review, we discuss the implication of AQPs in the clinical entities frequently encountered in ICUs, such as systemic inflammation and sepsis, ARDS, AKI, and brain edema due to different types of primary brain injury from a clinical perspective. Current and possible future therapeutic implications are also considered.