Author:
Dubey Apurva,Acharya Sourya,Shukla Samarth,Kumar Sunil
Abstract
The Chinese centre for disease control and prevention detected a novel severe acute respiratory syndrome - coronavirus 2 (SARS - CoV2) from a nasopharyngeal swab in a patient with atypical pneumonia in Wuhan, Hubei province, China on January, 2020.1 Corona virus disease-19 (COVID-19) has a high mortality rate in critically ill patients. Acute heart injury, acute kidney injury and sudden thromboembolic events are becoming more common and they can occur regardless of pulmonary or respiratory symptoms.1-5 COVID-19 has been shown to have the ability to create a hypercoagulable state in recent studies.2,3,6,7 Viral infections can cause endothelial cell dysfunction, resulting in excessive throbbing production and fibrinolysis inhibition.8- 10 Hypoxia is also linked to an increase in blood viscosity and the activation of hypoxia-related genes that regulate coagulation and fibrinolysis making thrombotic events more likely.11,12 This septic-like coagulopathy can also lead to venous thrombosis, pulmonary embolism, and, in the worst-case scenario, disseminated intravascular coagulation.3,4 Cerebral venous thrombosis, in particular, can manifest itself in a wide range of neurologic signs and symptoms.13,14 and had consistently fatal results.
Publisher
Akshantala Enterprises Private Limited