Prevalence of Pulmonary Embolism in COVID-19: a Pooled Analysis

Abstract

There remains a high risk of thrombosis in patients affected by the SARS-CoV-2 virus and recent reports have shown pulmonary embolism (PE) as a cause of sudden death in these patients. However, the pooled rate of this deadly and frequently underdiagnosed condition among COVID-19 patients remains largely unknown. Given the frequency with which pulmonary embolism has been reported as a fatal complication of severe coronavirus disease, we sought to ascertain the actual prevalence of this event in COVID-19 patients. Using PubMed/Medline, EMBASE, and SCOPUS, a thorough literature search was performed to identify the studies reporting rate of PE among COVID-19. Random effects models were obtained to perform a meta-analysis, and I 2 statistics were used to measure inter-study heterogeneity. Among 3066 COVID-19 patients included from 9 studies, the pooled prevalence of PE was 15.8% (95% CI (6.0–28.8%), I 2 = 98%). The pooled rate in younger cohort (age < 65 years) showed a higher prevalence of 20.5% (95% CI (17.6–24.8%)) as compared to studies including relatively older cohort (age > 65 years) showing 14.3% (95% CI (2.9–30.1%)) ( p < 0.05). Single-center studies showed a prevalence of 12.9% (95% CI 1.0–30.2%), while that of multicenter studies was 19.5% (95% CI 14.9–25.2%) ( p < 0.05). Pulmonary embolism is a common complication of severe coronavirus disease and a high degree of clinical suspicion for its diagnosis should be maintained in critically ill patients.

Endothelium Infection and Dysregulation by SARS-CoV-2: Evidence and Caveats in COVID-19

“…Microvascular thrombosis is characteristic of severe COVID-19 [ 10 , 14 , 15 , 16 , 28 ] and it has been proposed that a virus-induced prothrombotic state culminates with hyperinflammatory effectors and platelets to form immunothrombotic clots [ 152 , 153 ]. Reports of microangiopathic complications in severe COVID-19—including disseminated intravascular coagulation (DIC), venous thromboembolism, and pulmonary embolism—support a role for immunothrombosis in viral pathogenesis [ 22 , 23 , 154 ].…”

“…SARS-CoV-2 may thus cause endothelial dysfunction either directly through endothelial cell infection, or indirectly through the infection of other susceptible cell types, which cause hyperinflammation and aberrant antiviral responses [ 14 , 17 , 27 ]. Endothelial damage is an important culprit in multi-organ immunothrombosis and contributes to severe COVID-19 disease progression [ 10 , 14 , 15 , 16 , 28 ].…”

Radiological analysis of acute pulmonary thromboembolism as a consequence of COVID-19: A case report

“…The case report deals with a patient infected with SARS-CoV-2 who developed acute PE and died eight days after seeking medical care due to symptoms related to COVID-19. Due to the underlying thrombotic -pro-inflammatory and hypercoagulable -environment characteristic of this viral infection, patients with COVID-19 are highly predisposed to pulmonary embolism [4] . The patient had some comorbidities that are related to obesity in the SARS-CoV-2 infection.…”

“…In more severe cases, it stands out the patient's tendency to evolve to a hyperinflammatory and hypercoagulant state that may culminate in the formation of venous and arterial thrombi, with emphasis on Pulmonary Embolism (PE). This can have a varied presentation, from asymptomatic to chest pain, dyspnea, hemoptysis and syncope [4] . The hypercoagulation present in patients with COVID-19 can be influenced by several mechanisms such as severe hypoxia, pre-existing comorbidities, and dysfunctions associated with systemic functioning that compromise hemostatic homeostasis [5] .…”

“…The hypercoagulation present in patients with COVID-19 can be influenced by several mechanisms such as severe hypoxia, pre-existing comorbidities, and dysfunctions associated with systemic functioning that compromise hemostatic homeostasis [5] . Studies indicate that infection alone, without the presence of associated risk factors, considerably increases the risk of PE, since patients infected with SARS-CoV-2 in severe stages have the three factors attributed to thrombosis, known as Virchow's triad (endothelial injury, reduced flow, hypercoagulation state) [4,6] . In laboratory tests, the propensity to clots is perceived by the increase in the levels of Ddimer, fibrinogen and other products of fibrin degradation -the first being an important marker not only for screening the diagnosis, but also for the patient's prognosis [6,7] .…”