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Review
. 2021 Mar 4;10(5):1064.
doi: 10.3390/jcm10051064.

SARS-CoV-2 Infection: Modulator of Pulmonary Embolism Paradigm

Affiliations
Review

SARS-CoV-2 Infection: Modulator of Pulmonary Embolism Paradigm

Mohammad Suhail Akhter et al. J Clin Med. .

Abstract

Pulmonary embolism (PE) is a life-threatening complication arising from venous thromboembolism with a difficult diagnosis and treatment and is often associated with increased mortality and morbidity. PE had a significantly low incidence prior to the COVID-19 epidemic. This condition saw a sharp surge during the COVID-19 pandemic, indicating an evident viral influence on PE's pathophysiology in COVID-19 patients. The hypercoagulable state induced by the viral load seems to be the major contributor, and the classical causative factors seem to play a lesser role. PE in COVID-19 infection has become a mammoth challenge since the diagnosis is quite challenging due to overlapping symptoms, lack of prior-known predisposing risk factors, limited resources, and viral transmittance risk. Numerous factors arising out of the viral load or treatment lead to an increased risk for PE in COVID-19 patients, besides the fact that certain unknown risk factors may also contribute to the incidence of PE in COVID-19 patients. The management of PE in COVID-19 infection mainly comprises thromboprophylaxis and anticoagulant therapy with mechanical ventilation, depending on the risk stratification of the patient, with a post-COVID-19 management that prevents recurrent PE and complications. This review aims to discuss various aspects of COVID-19-infection-associated PE and major differential aspects from non-COVID-19 PE.

Keywords: COVID-19; inflammation; pulmonary embolism; thrombosis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The above figure illustrates how the SARS-CoV-2 virus sets off a series of chain reactions in the intracellular and extracellular spaces of cells of the vasculature lining the alveolar space. This simultaneously sets into motion coagulation, inflammation, and complement-based pathways, resulting in a hypercoagulable state and a cytokine storm that worsens the clinical state of the individual. As is apparent from the figure, each pathway feeds into the enhancement of the other.

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