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The Covid-19 pandemic has pushed many hospitals to their capacity limits. Therefore, a triage of patients has been discussed controversially primarily through an ethical perspective. The term triage contains many aspects such as urgency of treatment, severity of the disease and pre-existing conditions, access to critical care, or the classification of patients regarding subsequent clinical pathways starting from the emergency department. The determination of the pathways is important not only for patient care, but also for capacity planning in hospitals. We examine the performance of a human-made triage algorithm for clinical pathways which is considered a guideline for emergency departments in Germany based on a large multicenter dataset with over 4,000 European Covid-19 patients from the LEOSS registry. We find an accuracy of 28 percent and approximately 15 percent sensitivity for the ward class. The results serve as a benchmark for our extensions including an additional category of palliative care as a new label, analytics, AI, XAI, and interactive techniques. We find significant potential of analytics and AI in Covid-19 triage regarding accuracy, sensitivity, and other performance metrics whilst our interactive human-AI algorithm shows superior performance with approximately 73 percent accuracy and up to 76 percent sensitivity. The results are independent of the data preparation process regarding the imputation of missing values or grouping of comorbidities. In addition, we find that the consideration of an additional label palliative care does not improve the results.

Background and purpose During acute coronavirus disease 2019 (COVID‐19) infection, neurological signs, symptoms and complications occur. We aimed to assess their clinical relevance by evaluating real‐world data from a multinational registry. Methods We analyzed COVID‐19 patients from 127 centers, diagnosed between January 2020 and February 2021, and registered in the European multinational LEOSS (Lean European Open Survey on SARS‐Infected Patients) registry. The effects of prior neurological diseases and the effect of neurological symptoms on outcome were studied using multivariate logistic regression. Results A total of 6537 COVID‐19 patients (97.7% PCR‐confirmed) were analyzed, of whom 92.1% were hospitalized and 14.7% died. Commonly, excessive tiredness (28.0%), headache (18.5%), nausea/emesis (16.6%), muscular weakness (17.0%), impaired sense of smell (9.0%) and taste (12.8%), and delirium (6.7%) were reported. In patients with a complicated or critical disease course (53%) the most frequent neurological complications were ischemic stroke (1.0%) and intracerebral bleeding (ICB; 2.2%). ICB peaked in the critical disease phase (5%) and was associated with the administration of anticoagulation and extracorporeal membrane oxygenation (ECMO). Excessive tiredness (odds ratio [OR] 1.42, 95% confidence interval [CI] 1.20–1.68) and prior neurodegenerative diseases (OR 1.32, 95% CI 1.07–1.63) were associated with an increased risk of an unfavorable outcome. Prior cerebrovascular and neuroimmunological diseases were not associated with an unfavorable short‐term outcome of COVID‐19. Conclusion Our data on mostly hospitalized COVID‐19 patients show that excessive tiredness or prior neurodegenerative disease at first presentation increase the risk of an unfavorable short‐term outcome. ICB in critical COVID‐19 was associated with therapeutic interventions, such as anticoagulation and ECMO, and thus may be an indirect complication of a life‐threatening systemic viral infection., We retrospectively analyzed data from 6537 predominantly hospitalized COVID‐19 patients registered in the European multinational Lean European Open Survey on SARS‐Infected Patients (LEOSS) registry between January 2020 and February 2021. Common neurological symptoms were excessive tiredness (28.0%), headache (18.5%), nausea/emesis (16.6%), muscular weakness (17.0%), impaired sense of smell (9.0%) and taste (12.8%), and delirium (6.7%). Most frequent neurological complications were ischemic stroke (1.0%) and intracerebral bleeding (2.2%) in patients with a complicated or critical disease course. Excessive tiredness (odds ratio [OR] 1.42) and prior neurodegenerative disease (OR 1.32) were associated with an increased risk of an unfavorable outcome.

Purpose The ongoing pandemic caused by the novel severe acute respiratory coronavirus 2 (SARS-CoV-2) has stressed health systems worldwide. Patients with chronic kidney disease (CKD) seem to be more prone to a severe course of coronavirus disease (COVID-19) due to comorbidities and an altered immune system. The study’s aim was to identify factors predicting mortality among SARS-CoV-2-infected patients with CKD. Methods We analyzed 2817 SARS-CoV-2-infected patients enrolled in the Lean European Open Survey on SARS-CoV-2-infected patients and identified 426 patients with pre-existing CKD. Group comparisons were performed via Chi-squared test. Using univariate and multivariable logistic regression, predictive factors for mortality were identified. Results Comparative analyses to patients without CKD revealed a higher mortality (140/426, 32.9% versus 354/2391, 14.8%). Higher age could be confirmed as a demographic predictor for mortality in CKD patients (> 85 years compared to 15–65 years, adjusted odds ratio (aOR) 6.49, 95% CI 1.27–33.20, p = 0.025). We further identified markedly elevated lactate dehydrogenase (> 2 × upper limit of normal, aOR 23.21, 95% CI 3.66–147.11, p p = 0.002), anemia (Hb p = 0.024), and C-reactive protein (≥ 30 mg/l, aOR 3.44, 95% CI 1.13–10.45, p = 0.029) as predictors, while renal replacement therapy was not related to mortality (aOR 1.15, 95% CI 0.68–1.93, p = 0.611). Conclusion The identified predictors include routinely measured and universally available parameters. Their assessment might facilitate risk stratification in this highly vulnerable cohort as early as at initial medical evaluation for SARS-CoV-2.

Diabetes mellitus Typ 2 stellt einen wichtigen Risikofaktor für atherosklerotische Erkrankungen wie Myokardinfarkt und ischämischen Schlaganfall dar. Dabei kommt es zu einer sehr frühen und diffusen Veränderung der Gefäße. Verschiedene Theorien können bis jetzt dieses erhöhte Risiko jedoch nicht vollständig erklären. Aufgrund der peripheren Insulinresistenz mit konsekutiv erhöhter Insulinausschüttung im Anfangsstadium dieser Erkrankung weisen die betroffenen Patienten zunächst einen erhöhten Blutspiegel an C-Peptid auf, das in äquimolarer Menge mit Insulin sezerniert wird. C-Peptid galt bis vor einiger Zeit als biologisch inert. Studien der letzten Jahre konnten jedoch sowohl in vitro als auch in vivo zahlreiche Effekte dieser Substanz zeigen. Monozyten spielen in der Frühphase der Entstehung atherosklerotischer Plaques eine wichtige Rolle, indem sie durch verschiedene Chemotaxine angelockt werden und in die Gefäßwand einwandern. Chemotaktisch wirkende Stoffe werden entweder durch Zellen der Gefäßwand gebildet oder insudieren in sie im Rahmen der endothelialen Dysfunktion und gesteigerten Permeabilität. Die vorliegende Studie untersuchte den chemotaktischen Einfluss von C-Peptid auf Monozyten. Es konnte gezeigt werden, dass C-Peptid in vitro dosisabhängig chemotaktisch auf humane Monozyten wirkt. Dieser Effekt wird vermutlich über Phospho-Inositol-3-Kinase (PI3K) vermittelt. Weder Mitogen-activated protein kinase (MAPK) noch G-Proteine noch Proteinkinase C (PKC) scheinen beteiligt zu sein. Die durch C-Peptid induzierte Migration konnte durch Aktivatoren der nukleären Transkriptionsfaktoren Peroxisome proliferator-activated receptor (PPAR)ð alpha und gamma nicht signifikant gehemmt werden. Die Ergebnisse legen eine Beteiligung von C-Peptid Ablagerungen in der Gefäßintima von Typ-2-Diabetikern an der Rekrutierung von Monozyten nahe. Dies könnte als früher Schritt in der Atherogenese dieser Patienten eine bedeutende Rolle spielen.