Recent studies suggest that thrombotic complications are a common phenomenon in the novel SARS-CoV-2 infection. The main objective of our study is to assess cumulative incidence of pulmonary embolism (PE) in non critically ill COVID-19 patients and to identify its predicting factors associated to the diagnosis of pulmonary embolism. We retrospectevely reviewed 452 electronic medical records of patients admitted to Internal Medicine Department of a secondary hospital in Madrid during Covid 19 pandemic outbreak. We included 91 patients who underwent a multidetector Computed Tomography pulmonary angiography(CTPA) during conventional hospitalization. The cumulative incidence of PE was assessed ant the clinical, analytical and radiological characteristics were compared between patients with and without PE. PE incidence was 6.4% (29/452 patients). Most patients with a confirmed diagnosed with PE recieved low molecular weight heparin (LMWH): 79.3% (23/29). D-dimer peak was significatly elevated in PE vs non PE patients (14,480 vs 7230 mcg/dL, p = 0.03). In multivariate analysis of patients who underwent a CTPA we found that plasma D-dimer peak was an independen predictor of PE with a best cut off point of > 5000 µg/dl (OR 3.77; IC95% (1.18-12.16), p = 0.03). We found ninefold increased risk of PE patients not suffering from dyslipidemia (OR 9.06; IC95% (1.88-43.60). Predictive value of AUC for ROC is 75.5%. We found a high incidence of PE in non critically ill hospitalized COVID 19 patients despite standard thromboprophylaxis. An increase in D-dimer levels is an independent predictor for PE, with a best cutoff point of > 5000 µg/ dl.

Background The COVID‐19 outbreak has affected almost all hospital departments, including transfusion services. However, the demand for transfusions in a general hospital designated to deal with COVID‐19 patients has not been analysed before. Study Design and Methods A retrospective study was conducted to evaluate blood transfusion practices from 15 March to 14 April 2020 at Hospital Universitario Infanta Leonor (Madrid, Spain). During this month, with few exceptions, the hospital became a ‘COVID‐19’ centre. In addition, transfusion rates during this time frame and the same period over the last 4 years were compared. Results From 15 March to 14 April 2020, only 254 blood components were transfused, resulting in a 49·3% reduction over the previous year. Interestingly, in critically ill patients, the red blood cell (RBC) transfusion/bed ratio significantly decreased during this period (0·92) compared to the same ratio over the past 4 years (2·70) (P = 0·02). Of note, 106 blood components (95 RBC; 11 platelet concentrates) were transfused to only 36 out of 1348 COVID‐19 patients (2·7%). The main reason for RBC transfusion in COVID‐19 patients was a previous underlying disease (44%) followed by bleeding (25%) and inflammatory anaemia (25%). Conclusion This is the first study to report a decrease in blood transfusions during the COVID‐19 pandemic in a general hospital and especially in the intensive care unit. The results of this study suggest that COVID‐19 does not generally induce transfusion requiring anaemia, being the main causes for transfusion in these patients underlying conditions or bleeding.

Background: The link between coagulation system disorders and COVID-19 has not yet been fully elucidated.Aim: Evaluating the association of non-previously reported coagulation proteins with COVID-19 severity and mortality.Design: Cross-sectional study of 134 COVID-19 patients recruited at admission and classified according to the highest COVID-19 severity reached (asymptomatic/mild, moderate, or severe) and 16 healthy control individuals.Methods: Coagulation proteins levels (antithrombin, prothrombin, factor_XI, factor_XII, and factor_XIII) and CRP were measured in plasma by the ProcartaPlex Panel (Invitrogen) multiplex immunoassay upon diagnosis.Results: We found higher levels of antithrombin, prothrombin, factor XI, factor XII, and factor XIII in asymptomatic/mild and moderate COVID-19 patients compared to healthy individuals. Interestingly, decreased levels of antithrombin and factors XI, XII, and XIII were observed in those patients who eventually developed severe illness. Additionally, survival models showed us that patients with lower levels of these coagulation proteins had an increased risk of death.Conclusion: COVID-19 provokes early increments of some specific coagulation proteins in most patients. However, lower levels of these proteins at diagnosis might “paradoxically” imply a higher risk of progression to severe disease and COVID-19-related mortality.

Background: Meta-analyses of observational studies report a 1.1-1.7% pooled risk of stroke among patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection requiring hospitalization, but consultations for stroke and reperfusion procedures have decreased during the outbreak that occurred during the first half of the year 2020. It is still unclear whether a true increase in the risk of stroke exists among patients with coronavirus disease 2019 . In-hospital ischemic stroke (IHIS) complicated the 0.04-0.06% of all admissions in the pre-COVID-19 era, but its incidence has not been assessed among inpatients with COVID-19. We aimed to compare IHIS incidence among patients with SARS-CoV-2 infection with that of inpatients with non-COVID-19 illnesses from the same outbreak period and from previous periods. Methods: This historical cohort study belongs to the COVID-19@Vallecas cohort. The incidence of IHIS was estimated for patients with SARS-CoV-2 hospitalized during March-April 2020 [COVID-19 cohort (CC)], for patients with non-COVID-19 medical illness hospitalized during the same outbreak period [2020 non-COVID-19 cohort (20NCC)], and for inpatients with non-COVID-19 illness admitted during March-April of the years 2016-2019 [historical non-COVID-19 cohort (HNCC)]. Unadjusted risk of IHIS was compared between the three cohorts, and adjusted incidence rate ratio (IRR) of IHIS between cohorts was obtained by means of Poisson regression.Results: Overall, 8126 inpatients were included in this study. Patients in the CC were younger and more commonly men than those from the HNCC and 20NCC. Absolute risk of IHIS was 0.05% for HNCC, 0.23% for 20NCC, and 0.36% for CC, (p = 0.004 for HNCC vs. CC). Cumulative incidence for IHIS by day nine after admission, with death as a competing risk, was 0.09% for HNCC, 0.23% for 20NCC, and 0.50% for CC. In an adjusted Poisson regression model with sex, age, needing of intensive care unit admission, and cohort (HNCC as reference) as covariates, COVID-19 was an independent predictor for IHIS (IRR 6.76, 95% confidence interval 1.66-27.54, p = 0.01). A nonsignificant increase in the risk of IHIS was observed for the 20NCC (IRR 5.62, 95% confidence interval 0.93-33.9, p = 0.06).Conclusions: SARS-CoV-2 outbreak was associated with an increase in the incidence of IHIS when compared with inpatients from a historical cohort. Viral infection itself may be related to the increased risk of IHIS among patients with COVID-19, but in view of our results from the 20NCC, it is likely that other factors, such as hospital saturation and overwhelming of health systems, may have played a role in the increased frequency of IHIS.

The link between coagulation system disorders and COVID-19 has not yet been fully elucidated. With the aim of evaluating the association of several coagulation proteins with COVID-19 severity and mortality, we performed a cross-sectional study in 134 patients classified according to the highest disease severity reached during the disease. We found higher levels of antithrombin, prothrombin, factor XI, factor XII and factor XIII in asymptomatic/mild and moderate COVID-19 patients than healthy individuals. Interestingly, decreased levels of antithrombin, factor XI, XII and XIII were observed in those patients who eventually developed severe illness. Additionally, survival models showed us that patients with lower levels of these coagulation proteins had an increased risk of death. In conclusion, COVID-19 provokes early increments of some specific coagulation proteins in most patients. However, lower levels of these proteins at diagnosis might 'paradoxically' imply a higher risk of progression to severe disease and COVID-19-related mortality.

La amiloidosis primaria es una enfermedad multisistémica debida al mal plegamiento de proteínas kappa o lambda. El pronóstico es infausto y el tratamiento emplea quimioterapia. La afectación hepática se describe en el 70% de las autopsias de pacientes con amiloidosis sistémica y se asocia a peor pronóstico. Presentamos el caso de un varón de 41 años de edad que debuta con edemas en miembros inferiores y bolsa escrotal y síndrome nefrótico clínico y bioquímico. La biopsia renal es compatible con una amiloidosis primaria. Inicia tratamiento quimioterápico logrando respuesta hematológica completa, pero, a pesar de ello, sufre un fallo hepático fulminante de origen colestásico, y fallece.