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Since the beginning of the coronavirus disease 2019 (COVID-19) pandemic, the roll-out of vaccines and therapeutic agents, as well as the emergence of novel SARS-CoV-2 variants, have shown significant effects on disease severity. Patients hospitalized at our center between January 2020 and April 2022 were attributed to subgroups depending on which SARS-CoV-2 variant was predominantly circulating in Germany: (i) Wild-type: January 1, 2020, to March 7, 2021, (ii) Alpha variant: August 3, 2021, to June 27, 2021, (iii) Delta variant: June 28, 2021, to December 26, 2021, and (iv) Omicron variant: December 27, 2021, to April 30, 2022. Between January 2020 and April 2022, 1500 patients with SARS-CoV-2 infections were admitted to the University Medical Center Hamburg-Eppendorf. The rate of patients who were admitted to the intensive care unit (ICU) decreased from 31.2% (n = 223) in the wild-type group, 28.5% (n = 72) in the Alpha variant group, 18.8% (n = 67) in the Delta variant group, and 13.4% (n = 135) in the Omicron variant group. Also, in-hospital mortality decreased from 20.6% (n = 111) in the wild-type group, 17.5% (n = 30) in the Alpha variant group, 16.8% (n = 33) in the Delta variant group, and 6.6% (n = 39) in the Omicron variant group. The median duration of hospitalization was similar in all subgroups and ranged between 11 and 15 days throughout the pandemic. In-hospital mortality and rate of ICU admission among hospitalized COVID-19 patients steadily decreased throughout the pandemic. However, the practically unchanged duration of hospitalization demonstrates the persistent burden of COVID-19 on the healthcare system. [ABSTRACT FROM AUTHOR]

Background: Critically ill patients in intensive care units can frequently suffer from cardiac arrest (ICU-CA), the incidence of ICU-CA is associated with high mortality. Most studies on ICU-CA focused on risk factors and intra-arrest determinants. However, there is a lack of data on organ failure after ICU-CA and its clinical implications for outcome. This study aimed to investigate ICU-CA incidence, outcome and the occurrence of organ failure after ICU-CA.Methods: We conducted a prospective observational study over a 1-year at 12 intensive care units of a tertiary care university hospital. We included all consecutive adult patients suffering cardiac arrest (CA) during the ICU stay. Incidence, clinical and neurological outcome, as well as organ failure and support were assessed.Results: Out of 7690 patients, 176 (2%) with ICU-CA were identified during the study period. Male patients comprised 63% and the median age was 70 (58-78) years. The median ICU stay before ICU-CA was 3 (1-8) days. The initial cardiac rhythm was shockable (VT/VF) in 23% of patients; defibrillation during CPR was performed in 19%. The presumed cause of CA was cardiac in 24%, and sustained ROSC was observed in 80% of patients. Before CA 57% (n = 100) of patients were sedated, 63% (n = 110) mechanically ventilated, 70% needed vasopressor therapy and renal replacement therapy was necessary in 27% (n = 48) of patients. Organ failure after ICU-CA was common, 70% suffered from post-CA cardiac failure, renal replacement therapy was newly initiated in 26% of patients and liver failure occurred in 24% of patients. Mortality at ICU-discharge and at hospital discharge was 66 % and 68 %, respectively. Multivariate regression analysis identified the SOFA score [HR 1.09, 95% CI (0.92-3.18); p < 0.05] and liver failure [HR 2.44, 95% CI (1.39-4.26); p < 0.001] after ICU-CA as independent predictors of mortality.Conclusion: The incidence of ICU-CA is rare in critically ill patients. Organ failure before and after ICU-CA is common; liver failure incidence and severity of illness after ICU-CA are independent predictors of mortality and should be considered in further decisions on ICU therapy. [ABSTRACT FROM AUTHOR]

Infection with the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) results in respiratory syndromes but also in vascular complications such as thromboembolism (TE). In this regard, immunothrombosis, resulting from inflammation in SARS-CoV-2 infected tissues, has been described. Data on TE in COVID-19 are mainly based on clinical observational and/or incomplete autopsy studies. The true burden of TE and the relevance of genetic predisposition, however, have not been resolved. Here, we report on a consecutive cohort of 100 fully autopsied patients deceased by SARS-CoV-2 infections during the first wave of the pandemic (March to April 2020). We investigated the localization of TE, potential clinical risk factors, and the prothrombotic gene mutations, factor V Leiden and prothrombin G20210A, in postmortem blood or tissue samples. TE was found in 43/100 autopsies. 93 % of TE events were venous occlusions, with 23 patients having pulmonary thromboembolism (PT) with or without lower-extremity deep vein thrombosis. Of these, 70 % showed PT restricted to (sub)segmental arteries, consistent with in situ immunothrombosis. Patients with TE had a significantly higher BMI and died more frequently at an intensive care unit. Hereditary thrombophilia factors were not associated with TE. Our autopsy results show that a significant proportion of SARS-CoV-2 infected patients suffer from TE, affecting predominantly the venous system. Orthotopic peripheral PT was the most frequent finding. Hereditary thrombophilia appears not to be a determinant for TE in COVID-19. However, obesity and the need for intensive care increase the risk of TE in these patients. [Display omitted] • TE was found in almost half of those who died of COVID-19 in the first wave. • Obesity and intensive care are risk factors for COVID-19 associated TE. • Hereditary thrombophilia appears not to contribute to TE in lethal COVID-19. [ABSTRACT FROM AUTHOR]

Hepatopulmonary syndrome (HPS) occurs in 20-30% of patients with liver cirrhosis and is associated with a >2 fold increased mortality. Endothelial dysfunction seems to play a central role in its pathogenesis. von Willebrand factor antigen (vWF-Ag), an established marker of endothelial dysfunction, is significantly elevated in patients with liver cirrhosis, portal hypertension, and in experimental HPS. Aim of the present study was to evaluate the impact of vWF-Ag as a screening marker for presence of HPS in patients with stable cirrhosis. Methods 145 patients with stable liver cirrhosis were screened for presence of HPS in this prospective cohort type cross sectional diagnostic study. vWF-Ag and SaO2 levels were assessed at time of screening for HPS. Criteria of HPS were fulfilled in 31 (21%) patients. Results vWF-Ag levels were significantly higher in patients with HPS compared to patients without HPS (p<0.001). Furthermore, vWF-Ag correlated significantly with gas exchange in HPS positive patients (p<0.05). vWF-Ag is an independent predictor of HPS after correction for sex, age, model for endstage-liver disease (MELD), and hepatic venous pressure gradient (HVPG) (OR per 1% increase of vWF-Ag: 1.02, 95% CI: 1.00-1.04, p<0.05). The best cut-off was 328% at a sensitivity of 100% and specificity of 53.5%; positive predictive value: 36.9%; negative predictive value: 100%. Conclusions HPS is associated with elevated vWF-Ag levels. vWF-Ag may be a useful screening tool for early detection of HPS. Further studies investigating vWF-Ag in HPS will be needed to confirm our findings. [ABSTRACT FROM AUTHOR]

Background & Aims: Hypoxic hepatitis (HH) is a frequent and life-threatening complication associated with states of oxygen depletion in critically ill patients. Ischemia and reperfusion contribute to liver injury in HH. Experimental data suggest beneficial effects of statins in hepatic ischemia/reperfusion injury. This study was conducted to investigate whether statin treatment prior to intensive care unit (ICU) admission affects incidence rates and severity of HH. Methods: Eight hundred fifty-one patients admitted consecutively to three medical ICUs between December 2008 and December 2009 were prospectively screened for new occurrence of HH within 48h following ICU admission. Statin treatment prior to ICU admission was assessed. 28-day-, 90-day-, and 1-year-survival as well as new-onset of complications in HH patients were prospectively documented. Results: Eighty-seven patients (10%) developed HH. Statin treatment prior to ICU admission was significantly associated with decreased incidence of HH within 48h after ICU admission in the multivariate analysis (adjusted OR=0.42 (95% CI 0.19–0.95); p <0.05). Cardiogenic shock (p <0.001), septic shock (p <0.001) and active alcohol consumption (p <0.01) were identified as independent risk factors for development of HH. 28-day-, 90-day-, and 1-year-mortality rates in HH were 58%, 67%, and 74%, respectively. Statins were associated with improved 28-day-survival in the total study cohort (p <0.05), but did not affect 90-day- and 1-year-mortality, respectively. Conclusions: Cardiogenic shock, septic shock, and active alcohol consumption were independent factors predisposing patients to new onset of HH. Statin treatment prior to ICU admission was the only protective factor regarding the new occurrence of HH in critically ill patients. [Copyright &y& Elsevier]