|D030341||Nidovirales Infections NIH||1.00|
|D003333||Coronaviridae Infections NIH||0.50|
|D012327||RNA Virus Infections NIH||0.50|
|D007154||Immune System Diseases NIH||0.41|
|D008171||Lung Diseases, NIH||0.26|
|D012140||Respiratory Tract Diseases NIH||0.24|
|D012141||Respiratory Tract Infections NIH||0.21|
|D011024||Pneumonia, Viral NIH||0.13|
|D014777||Virus Diseases NIH||0.12|
|D003141||Communicable Diseases NIH||0.09|
|D045169||Severe Acute Respiratory Syndrome NIH||0.05|
|D018352||Coronavirus Infections NIH||0.04|
There is one clinical trial.
The COVID-19 outbreak has led to a significant increase in the number of patients admitted to intensive care for respiratory distress. Early data indicate a particularly high risk of thrombotic risk to viral lung disease, particularly in the most severe patients, with a particularly high incidence of pulmonary embolism. Catheter thrombosis and extra-renal purification filters are also abnormally common. These thrombotic complications could contribute to the mortality observed in this pathology. The introduction of early curative anticoagulation in the most severe patients has just been proposed by the perioperative hemostasis interest group Biologically, a significant proportion of patients hospitalized in intensive care have a marked biological inflammatory syndrome, associated with signs of activation of clotting (a frank increase in D-dimers). The presence of circulating anticoagulants is common. Interestingly, thrombocytosis, normally observed in such inflammatory syndromes, is absent. In this context, it seems legitimate to explore these patients from a hemostasis perspective to identify the factors that cause this thrombotic over-risk, in order to minimize the occurrence of these complications.