COVID-19 and ECMO: the interplay between coagulation and inflammation-a narrative review.
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ABSTRACT:
SUBMITTER: Kowalewski M
PROVIDER: S-EPMC7209766 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The novel coronavirus disease (COVID-19) pandemic has caused an unprecedented worldwide socio-economic and health impact. There is increasing evidence that a combination of inflammation and hypercoagulable state are the main mechanisms of respiratory failure in these patients. This narrative review aims to summarize currently available evidence on the complex interplay of immune dysregulation, hypercoagulability, and thrombosis in the pathogenesis of respiratory failure in COVID-19 disease. In addition, we will describe the experience of anticoagulation and anti-inflammatory strategies that have been tested. Profound suppression of the adaptive and hyperactivity of innate immune systems with macrophage activation appears to be a prominent feature in this infection. Immune dysregulation together with endotheliitis and severe hypercoagulability results in thromboinflammation and microvascular thrombosis in the pulmonary vasculature leading to severe respiratory distress. Currently, some guidelines recommend the use of prophylactic low molecular weight heparin in all hospitalized patients, with intermediate dose prophylaxis in those needing intensive care, and the use of therapeutic anticoagulation in patients with proven or suspected thrombosis. Strong recommendations cannot be made until this approach is validated by trial results. To target the inflammatory cascade, low-dose dexamethasone appears to be helpful in moderate to severe cases and trials with anti-interleukin agents (e.g., tocilizumab, anakinra, siltuximab) and non-steroidal anti-inflammatory drugs are showing early promising results. Potential newer agents (e.g., Janus kinase inhibitor such as ruxolitinib, baricitinib, fedratinib) are likely to be investigated in clinical trials. Unfortunately, current trials are mostly examining these agents in isolation and there may be a significant delay before evidence-based practice can be implemented. It is plausible that a combination of anti-viral drugs together with anti-inflammatory and anti-coagulation medicines will be the most successful strategy in managing severely affected patients with COVID-19.
| S-EPMC7446744 | biostudies-literature
Project description:BackgroundCoronavirus disease 2019 (COVID-19) is the etiology of acute respiratory distress syndrome (ARDS). Extracorporeal membrane oxygenation (ECMO) is used to support gas exchange in patients who have failed conventional mechanical ventilation. However, there is no clear consensus on the timing of ECMO use in severe COVID-19 patients.ObjectiveThe aim of this study is to compare the differences in pre-ECMO time and ECMO duration between COVID-19 survivors and non-survivors and to explore the association between them.MethodsPubMed, the Cochrane Library, Embase, and other sources were searched until 21 October 2022. Studies reporting the relationship between ECMO-related time and COVID-19 survival were included. All available data were pooled using random-effects methods. Linear regression analysis was used to determine the correlation between pre-ECMO time and ECMO duration. The meta-analysis was registered with PROSPERO under registration number CRD42023403236.ResultsOut of the initial 2473 citations, we analyzed 318 full-text articles, and 54 studies were included, involving 13,691 patients. There were significant differences between survivors and non-survivors in the time from COVID-19 diagnosis (standardized mean difference (SMD) = -0.41, 95% confidence interval (CI): [-0.53, -0.29], p < 0.00001), hospital (SMD = -0.53, 95% CI: [-0.97, -0.09], p = 0.02) and intensive care unit (ICU) admission (SMD = -0.28, 95% CI: [-0.49, -0.08], p = 0.007), intubation or mechanical ventilation to ECMO (SMD = -0.21, 95% CI: [-0.32, -0.09], p = 0.0003) and ECMO duration (SMD = -0.18, 95% CI: [-0.30, -0.06], p = 0.003). There was no statistical association between a longer time from symptom onset to ECMO (hazard ratio (HR) = 1.05, 95% CI: [0.99, 1.12], p = 0.11) or time from intubation or mechanical ventilation (MV) and the risk of mortality (highest vs. lowest time groups odds ratio (OR) = 1.18, 95% CI: [0.78, 1.78], p = 0.42; per one-day increase OR = 1.14, 95% CI: [0.86, 1.52], p = 0.36; HR = 0.99, 95% CI: [0.95, 1.02], p = 0.39). There was no linear relationship between pre-ECMO time and ECMO duration.ConclusionThere are differences in pre-ECMO time between COVID-19 survivors and non-survivors, and there is insufficient evidence to conclude that longer pre-ECMO time is responsible for reduced survival in COVID-19 patients. ECMO duration differed between survivors and non-survivors, and the timing of pre-ECMO does not have an impact on ECMO duration. Further studies are needed to explore the association between pre-ECMO and ECMO time in the survival of COVID-19 patients.
| S-EPMC10856383 | biostudies-literature
Project description:Coronavirus disease 2019 is characterized by its severe respiratory effects. Data early on indicated an increased risk of mortality in patients with cardiovascular comorbidities. Early reports highlighted the multisystem inflammatory syndrome, cytokine storm, and thromboembolic events as part of the disease processes. The aim of this review is to assess the association between COVID-19 and its thrombotic complications, specifically related to the cardiovascular system. The role of neutrophil extracellular traps (NETs) is explored in the pathogenesis of the disease. The structure and anatomy of the virus are pivotal to its virulence in comparison to other α and β Coronaviridae (HCoV-229E, HCoV-OC43, HCoV-229E, HCoV-NL63, HCoV-OC43, and HCoV-HKU1). In particular, the host interaction and response may explain the variability of severity in patients. Angio tensin-converting enzyme 2 (ACE2) activation may be implicated in the cardiovascular and throm bogenic potential of the disease. The virus may also have direct effects on the endothelial lining affecting hemostasis and resulting in thrombosis through several mechanisms. Dipyridamole may have a therapeutic benefit in NET suppression. Therapeutic avenues should be concentrated on the different pathophysiological steps involving the virus and the host.
| S-EPMC8945192 | biostudies-literature
Project description:Coronavirus disease 2019 (COVID-19), caused by a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can cause life-threatening pathology characterized by a dysregulated immune response and coagulopathy. While respiratory failure induced by inflammation is the most common cause of death, micro-and macrovascular thrombosis leading to multiple organ failure are also causes of mortality. Dysregulation of systemic inflammation observed in severe COVID-19 patients is manifested by cytokine release syndrome (CRS) - the aberrant release of high levels of proinflammatory cytokines, such as IL-6, IL-1, TNFα, MP-1, as well as complement. CRS is often accompanied by activation of endothelial cells and platelets, coupled with perturbation of the balance between the pro-and antithrombotic mechanisms, resulting in thrombosis. Inflammation and thrombosis form a vicious circle, contributing to morbidity and mortality. Treatment of hyperinflammation has been shown to decrease thrombosis, while anti-thrombotic treatment also downregulates cytokine release. This review highlights the relationship between COVID-19-mediated systemic inflammation and thrombosis, the molecular pathways involved, the therapies targeting these processes, and the challenges currently encountered.
| S-EPMC9270234 | biostudies-literature
Project description:OBJECTIVE:To analyze the survival rates of patients with COVID-19 supported with extracorporeal membrane oxygenation (ECMO) and compare the survival rates of patients with COVID-19 supported with ECMO to patients with influenza supported with ECMO. DESIGN:A systematic review and meta-analysis to assess the impact of ECMO as supportive therapy of COVID-19. SETTING:The authors performed a search through the Cochrane, EMBASE, and MEDLINE/PubMed databases from inception to February 19, 2021, for studies reporting hospitalized patients with COVID-19 managed with ECMO. PARTICIPANTS:A total of 134 studies were selected, including 6 eligible for the comparative meta-analysis of COVID-19 versus influenza. INTERVENTIONS:The authors pooled the risk ratio and random effects model. MEASUREMENTS AND MAIN RESULTS:The primary endpoint was the overall mortality of patients with COVID-19 receiving ECMO. Of the total number of 58,472 patients with COVID-19 reported, ECMO was used in 4,044 patients. The analysis suggested an overall in-hospital mortality of 39% (95% CI 0.34-0.43). In the comparative analysis, patients with COVID-19 on ECMO had a higher risk ratio (RR) for mortality when compared to influenza patients on ECMO: 72/164 (44%) v 71/186 (38%) RR 1.34; 95% CI 1.05-1.71; p = 0.03. CONCLUSIONS:ECMO could be beneficial in patients with COVID-19, according to the authors' meta-analysis. The reported mortality rate was 39%. This systematic analysis can provide clinical advice in the current era and ongoing pandemic.
| S-EPMC8585556 | biostudies-literature
Project description:The COVID-19 pandemic has shaken the world since early 2020 and its health, social, economic, and societal negative impacts at the global scale have been catastrophic. Since the early days of the pandemic, development of safe and effective vaccines was judged to be the best possible tool to minimize the effects of this pandemic. Drastic public health measures were put into place to stop the spread of the virus, with the hope that vaccines would be available soon. Thanks to the extraordinary commitments of many organizations and individuals from around the globe and the collaborative effort of many international scientists, vaccines against COVID-19 received regulatory approval for emergency human use in many jurisdictions in less than a year after the identification of the viral sequence. Several of these vaccines have been in use for some time; however, the pandemic is still ongoing and likely to persist for the foreseeable future. This is due to many reasons including reduced compliance with public health restrictions, limited vaccine manufacturing/distribution capacity, high rates of vaccine hesitancy, and the emergence of new variants with the capacity to spread more easily and to evade current vaccines. Here we discuss the discovery and availability of COVID-19 vaccines and evolving issues around mass vaccination programs.
| S-EPMC8779282 | biostudies-literature
Project description:[Figure: see text].
| S-EPMC8547586 | biostudies-literature
Project description:ObjectiveThis narrative review aims to provide a detailed overview of pleural abnormalities in patients with coronavirus disease 19 or COVID-19.BackgroundSevere acute respiratory syndrome coronavirus 2 (SARS-Cov-2) is a novel beta coronavirus responsible for COVID-19. Although pulmonary parenchymal and vascular changes associated with COVID-19 are well established, pleural space abnormalities have not been the primary focus of investigations.MethodsNarrative overview of the medical literature regarding pleural space abnormalities in COVID-19. The appropriate manuscripts were identified by searching electronic medical databases and by hand searching the bibliography of the identified papers. Pleural abnormalities on transverse and ultrasound imaging are discussed. The incidence, clinical features, pathophysiology, and fluid characteristics of pleural effusion are reviewed. Studies reporting pneumothorax and pneumomediastinum are examined to evaluate for pathogenesis and prognosis. A brief comparative analysis of pleural abnormalities among patients with COVID-19, severe acute respiratory syndrome (SARS), and Middle Eastern respiratory syndrome (MERS) has been provided.ConclusionsRadiologic pleural abnormalities are common in COVID-19, but the incidence of pleural effusion appears to be low. Pneumothorax is rare and does not independently predispose the patient to worse outcomes. SARS-CoV-2 infects the pleural space; however, whether the pleural fluid can propagate the infection is unclear.
| S-EPMC8339774 | biostudies-literature
Project description:COVID-19 (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]) is associated with coagulopathy through numerous mechanisms. The reported incidence of venous thromboembolism (VTE) in hospitalized patients with COVID-19 has varied widely, and several meta-analyses have been performed to assess the overall prevalence of VTE. The novelty of this coronavirus strain along with its unique mechanisms for microvascular and macrovascular thrombosis has led to uncertainty as to how to diagnose, prevent, and treat thrombosis in patients affected by this virus. This review discusses the epidemiology and pathophysiology of thrombosis in the setting of SARS-CoV-2 infection along with an updated review on the preventative and treatment strategies for VTE associated with SARS-CoV-2 infection.
| S-EPMC8847419 | biostudies-literature
Project description:SARS-CoV-2 is the agent responsible for COVID-19. The infection can be dived into three phases: mild infection, the pulmonary phase and the inflammatory phase. Treatment options for the pulmonary phase include: Hydroxychloroquine, Remdesivir, Lopinavir/Ritonavir. The inflammatory phase includes therapeutic options like Tocilizumab, Anakinra, Baricitinib, Eculizumab, Emapalumab and Heparin. Human clinical trials are starting to show some results, in some cases like that of Remdesivir and corticosteroids these are controversial. Coagulopathy is a common complication in severe cases, inflammation and coagulation are intertwined and cross-talking between these two responses is known to happen. A possible amplification of this cross-talking is suggested to be implicated in the severe cases that show both a cytokine storm and coagulopathy.
| S-EPMC7305708 | biostudies-literature