(1) Introduction: According to recent studies, the ratio of C-reactive-protein to lymphocyte is more sensitive and specific than other biomarkers associated to systemic inflammatory processes. This study aimed to determine the prognostic value of CLR on COVID-19 severity and mortality at emergency department (ED) admission. (2) Methods: Between 1 March and 30 April 2020, we carried out a multicenter and retrospective study in six major hospitals of northeast France. The cohort was composed of patients hospitalized for a confirmed diagnosis of moderate to severe COVID-19. (3) Results: A total of 1,035 patients were included in this study. Factors associated with infection severity were the CLR (OR: 1.001, CI 95%: (1.000–1.002), p = 0.012), and the lymphocyte level (OR: 1.951, CI 95%: (1.024–3.717), p = 0.042). In multivariate analysis, the only biochemical factor significantly associated with mortality was lymphocyte rate (OR: 2.308, CI 95%: (1.286–4.141), p = 0.005). The best threshold of CLR to predict the severity of infection was 78.3 (sensitivity 79%; specificity 47%), and to predict mortality, was 159.5 (sensitivity 48%; specificity 70%). (4) Conclusion: The CLR at admission to the ED could be a helpful prognostic biomarker in the early screening and prediction of the severity and mortality associated with SARS-CoV-2 infection.

Introduction: For the past two years, healthcare systems worldwide have been battling the ongoing COVID-19 pandemic. Several studies tried to find predictive factors of mortality in COVID-19 patients. We aimed to research age as a predictive factor associated with in-hospital mortality in severe and critical SARS-CoV-2 infection. Methods: Between 1 March and 20 April 2020, we conducted a multicenter and retrospective study on a cohort of severe COVID-19 patients who were all hospitalized in the Intensive Care Unit (ICU). We led our study in nine hospitals of northeast France, one of the pandemic’s epicenters in Europe. Results: The median age of our study population was 66 years (58–72 years). Mortality was 24.6% (CI 95%: 20.6–29%) in the ICU and 26.5% (CI 95%: 22.3–31%) in the hospital. Non-survivors were significantly older (69 versus 64 years, p < 0.001) than the survivors. Although a history of cardio-vascular diseases was more frequent in the non-survivor group (p = 0.015), other underlying conditions and prior level of autonomy did not differ between the two groups. On multivariable analysis, age appeared to be an interesting predictive factor of in-hospital mortality. Thus, age ranges of 65 to 74 years (OR = 2.962, CI 95%: 1.231–7.132, p = 0.015) were predictive of mortality, whereas the group of patients aged over 75 years was not (OR = 3.084, CI 95%: 0.952–9.992, p = 0.06). Similarly, all comorbidities except for immunodeficiency (OR = 4.207, CI 95%: 1.006–17.586, p = 0.049) were not predictive of mortality. Finally, survival follow-up was obtained for the study population. Conclusion: Age appears to be a relevant predictive factor of in-hospital mortality in cases of severe or critical SARS-CoV-2 infection.

Introduction: The COVID-19 outbreak had a major impact on healthcare systems worldwide. Our study aims to describe the characteristics and therapeutic emergency mobile service (EMS) management of patients with vital distress due to COVID-19, their in-hospital care pathway and their in-hospital outcome. Methods: This retrospective and multicentric study was conducted in the six main centers of the French Greater East region, an area heavily impacted by the pandemic. All patients requiring EMS dispatch and who were admitted straight to the intensive care unit (ICU) were included. Clinical data from their pre-hospital and hospital management were retrieved. Results: We included a total of 103 patients (78.6% male, median age 68). In the initial stage, patients were in a critical condition (median oxygen saturation was 72% (60–80%)). In the field, 77.7% (CI 95%: 71.8–88.3%) were intubated. Almost half of our population (45.6%, CI 95%: 37.1–56.9%) had clinical Phenotype 1 (silent hypoxemia), while the remaining half presented Phenotype 2 (acute respiratory failure). In the ICU, a great number had ARDS (77.7%, CI 95% 71.8–88.3% with a PaO₂/FiO₂ < 200). In-hospital mortality was 33% (CI 95%: 24.6–43.3%). The two phenotypes showed clinical and radiological differences (respiratory rate, OR = 0.98, p = 0.02; CT scan lesion extension >50%, OR = 0.76, p < 0.03). However, no difference was found in terms of overall in-hospital mortality (OR = 1.07, p = 0.74). Conclusion: The clinical phenotypes appear to be very distinguishable in the pre-hospital field, yet no difference was found in terms of mortality. This leads us to recommend an identical management in the initial phase, despite the two distinct presentations.

Introduction: Understanding hypoxemia, with and without the clinical signs of acute respiratory failure (ARF) in COVID-19, is key for management. Hence, from a population of critical patients admitted to the emergency department (ED), we aimed to study silent hypoxemia (Phenotype I) in comparison to symptomatic hypoxemia with clinical signs of ARF (Phenotype II). Methods: This multicenter study was conducted between 1 March and 30 April 2020. Adult patients who were presented to the EDs of nine Great-Eastern French hospitals for confirmed severe or critical COVID-19, who were then directly admitted to the intensive care unit (ICU), were retrospectively included. Results: A total of 423 critical COVID-19 patients were included, out of whom 56.1% presented symptomatic hypoxemia with clinical signs of ARF, whereas 43.9% presented silent hypoxemia. Patients with clinical phenotype II were primarily intubated, initially, in the ED (46%, p < 0.001), whereas those with silent hypoxemia (56.5%, p < 0.001) were primarily intubated in the ICU. Initial univariate analysis revealed higher ICU mortality (29.2% versus 18.8%, p < 0.014) and in-hospital mortality (32.5% versus 18.8%, p < 0.002) in phenotype II. However, multivariate analysis showed no significant differences between the two phenotypes regarding mortality and hospital or ICU length of stay. Conclusions: Silent hypoxemia is explained by various mechanisms, most physiological and unspecific to COVID-19. Survival was found to be comparable in both phenotypes, with decreased survival in favor of Phenotype II. However, the spectrum of silent to symptomatic hypoxemia appears to include a continuum of disease progression, which can brutally evolve into fatal ARF.