Articles: pandemics.
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Coronavirus Disease 2019 (COVID-19) threatens to overwhelm our medical infrastructure at the regional level causing spikes in mortality rates because of shortages of critical equipment, like ventilators. Fortunately, with the recent development and widespread deployment of small-scale manufacturing technologies like RepRap-class 3-D printers and open source microcontrollers, mass distributed manufacturing of ventilators has the potential to overcome medical supply shortages. In this study, after providing a background on ventilators, the academic literature is reviewed to find the existing and already openly-published, vetted designs for ventilators systems. ⋯ With the considerably larger motivation of an ongoing pandemic, it is assumed these projects will garner greater attention and resources to make significant progress to reach a functional and easily-replicated system. There is a large amount of future work needed to move open source ventilators up to the level considered scientific-grade equipment, and even further work needed to reach medical-grade hardware. Future work is needed to achieve the potential of this approach by developing policies, updating regulations, and securing funding mechanisms for the development and testing of open source ventilators for both the current COVID19 pandemic as well as for future pandemics and for everyday use in low-resource settings.
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Int J Chron Obstruct Pulmon Dis · Jan 2020
Clinical Courses and Outcomes of Patients with Chronic Obstructive Pulmonary Disease During the COVID-19 Epidemic in Hubei, China.
In this study, we investigated the acute exacerbation and outcomes of COPD patients during the outbreak of COVID-19 and evaluated the prevalence and mortality of COPD patients with confirmed COVID-19. ⋯ Our findings imply that acute exacerbations and hospitalizations of COPD patients were infrequent during the COVID-19 pandemic. However, COVID-19 patients with pre-existing COPD had a higher risk of all-cause mortality.
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Clin. Appl. Thromb. Hemost. · Jan 2020
ReviewCOVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation.
The novel coronavirus infection (COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as adult respiratory syndrome, sepsis, coagulopathy, and death in a proportion of patients. Among other factors and direct viral effects, the increase in the vasoconstrictor angiotensin II, the decrease in the vasodilator angiotensin, and the sepsis-induced release of cytokines can trigger a coagulopathy in COVID-19. A coagulopathy has been reported in up to 50% of patients with severe COVID-19 manifestations. ⋯ Prophylactic LMWH has been recommended by the International Society on Thrombosis and Haemostasis (ISTH) and the American Society of Hematology (ASH), but the best effective dosage is uncertain. Adapted to the individual risk of thrombosis and the d-dimer value, higher doses can be considered, especially since bleeding events in COVID-19 are rare. Besides the anticoagulant effect of LMWH, nonanticoagulant properties such as the reduction in interleukin 6 release have been shown to improve the complex picture of coagulopathy in patients with COVID-19.
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Clin. Appl. Thromb. Hemost. · Jan 2020
ReviewViral Coagulopathy in Patients With COVID-19: Treatment and Care.
COVID-19 has proven to be particularly challenging given the complex pathogenesis of SARS-CoV-2. Early data have demonstrated how the host response to this novel coronavirus leads to the proliferation of pro-inflammatory cytokines, massive endothelial damage, and generalized vascular manifestations. While SARS-CoV-2 primarily targets the upper and lower respiratory tract, other organ systems are also affected. ⋯ Tissue plasminogen activator and other fibrinolytic modalities may also be helpful in the overall management. Catheter-directed thrombolysis can be used in patients developing pulmonary embolism. Further investigations are required to understand the molecular and cellular mechanisms involved in the pathogenesis of COVID-19-associated thrombotic complications.