COVID-19 displays diverse disease severities and symptoms. Elevated inflammation mediated by hypercytokinemia induces a detrimental dysregulation of immune cells. However, there is limited understanding of how SARS-CoV-2 pathogenesis impedes innate immune signaling and function against secondary bacterial infections. We assessed the influence of COVID-19 hypercytokinemia on the functional responses of neutrophils and monocytes upon bacterial challenges from acute and corresponding recovery COVID-19 ICU patients. We show that severe hypercytokinemia in COVID-19 patients correlated with bacterial superinfections. Neutrophils and monocytes from acute COVID-19 patients showed severely impaired microbicidal capacity, reflected by abrogated ROS and MPO production as well as reduced NETs upon bacterial challenges. We observed a distinct pattern of cell surface receptor expression on both neutrophils and monocytes leading to a suppressive autocrine and paracrine signaling during bacterial challenges. Our data provide insights into the innate immune status of COVID-19 patients mediated by their hypercytokinemia and its transient effect on immune dysregulation upon subsequent bacterial infections

We present a case of an 80-year-old Turkish female patient with diabetes who suffered an acute myocardial infarction (AMI) and underwent percutaneous coronary balloon angioplasty (PTCA)/stenting. Due to new ischaemic episodes, a second PTCA/stenting had to be preformed 6 days later, which revealed a partial restent thrombosis. This case report raises several important issues. First, language problems are an important barrier for safety and quality in healthcare. Second, gender, ethnicity and age differences in patients with AMI need to be considered in order to eliminate inequities in clinical practice. Third, strategies to raise the awareness of cognitive biases as well as professional training about critical thinking and decision-making skills are needed.

Background: Veno-venous (VV) extracorporeal membrane oxygenation (ECMO) is increasingly used to support patients with severe acute respiratory distress syndrome (ARDS). In case of additional cardiocirculatory failure, some experienced centers upgrade the VV-ECMO with an additional arterial back ow cannula (termed VVA-ECMO). Here we analyzed short-and long-term outcome together with potential predictors of mortality.Methods: Retrospective analysis of outcome in VV ECMO patients with ARDS that received VVA upgrade due to acute cardio-circulatory deterioration from 2008-2021 at three ECMO referral centers.Results: We identi ed 73 VVA ECMO patients that either required an upgrade from VV to VVA (n=53) or were directly triple cannulated (n=20), most commonly for concomitant right-sided heart failure. Median (Interquartile Range) age was 49 (28-57) years and SOFA score was 14 (12-17) at VVA ECMO upgrade.ECMO support was required over 12 (6-22) days and ICU length of stay was 32 (16-46) days. Overall ICU mortality was 48% and hospital mortality 51%. Two additional patients died after hospital discharge while the remaining patients survived up to two years (with six patients being lost to follow-up). A SOFA score > 14 at the day of VVA upgrade and higher lactate level were independent predictors of mortality in the multivariate regression analysis.Conclusions: In this analysis, the use of VVA ECMO in patients with initial ARDS and concomitant cardiocirculatory failure was associated with a hospital survival of about 50%, and most of these patients survived up to 2 years. A SOFA score >14 and elevated lactate levels at the day of VVA upgrade predict unfavorable outcome.

Zusammenfassung. Als SIADH (Syndrom der inadäquaten ADH-Sekretion, Schwarz-Bartter-Syndrom) wird eine Elektrolytstörung aus dem Formenkreis der Hyponatriämie bezeichnet. Durch komplexe Mechanismen und verschiedene Ätiologien wird das im Hypothalamus gebildete, und im Hypophysenhinterlappen freigesetzte ADH (antidiuretisches Hormon) in inadäquat hohem Ausmass in die systemische Zirkulation freigesetzt. Nach Erreichen der renalen Sammelrohre führt das ADH zu einer der homöostatischen Situation unangemessenen Wasserretention, was konsekutiv eine hypoosmolare Hyponatriämie bewirkt. Mögliche Auslöser eines SIADH sind Medikamente, Neoplasien, Pneumopathien oder Pathologien des zentralen Nervensystems. Daneben können Operationen, Stress, Traumata, Schmerzen oder eine idiopathische Form zu diesem Syndrom führen. Die klinischen Symptome der Hyponatriämie sind mannigfaltig und häufig unspezifisch. Viele milde Formen verlaufen asymptomatisch. Bei schwererer Ausprägung der Elektrolytstörung treten Appetitlosigkeit, Nausea, Erbrechen, Muskelkrämpfe oder Wesensveränderungen auf. Extremformen mit komaähnlichen Zustandsbildern oder zerebralen Krampfanfällen werden heutzutage nur noch selten beobachtet. Die Differenzialdiagnose der Hyponatriämie ist breit und kann im klinischen Alltag nach definierten Abklärungsalgorithmen erfolgen. Therapeutisch bildet die Trinkmengenrestriktion den Hauptpfeiler der Behandlung.