Abstract
Preliminary evidence supports the notion that COVID-19 patients may have an increased susceptibility to develop venous thromboembolism (VTE). However, the magnitude of this association still needs to be defined. Furthermore, clinical predictors of thrombogenesis, and the relationship with the inflammatory status are currently unknown. On this basis, we conducted a retrospective, observational study on 259 consecutive COVID-19 patients admitted to an academic tertiary referral hospital in Northern Italy between March 19th and April 6th, 2020. Records of COVID-19 patients with a definite VTE event were reviewed for demographic information, co-morbidities, risk factors for VTE, laboratory tests, and anticoagulation treatment. Twenty-five cases among 259 COVID-19 patients developed VTE (9.6%), all of them having a Padua score > 4, although being under standard anticoagulation prophylaxis since hospital admission. In the VTE subcohort, we found a significant positive correlation between platelet count (PLT) and either C reactive protein (CRP) (p < 0.0001) or lactate dehydrogenase (LDH) (p = 0.0013), while a significant inverse correlation was observed between PLT and mean platelet volume (p < 0.0001). Platelet-to-lymphocyte ratio significantly correlated with CRP (p < 0.0001). The majority of VTE patients was male and younger compared to non-VTE patients (p = 0.002 and p = 0.005, respectively). No significant difference was found in d-dimer levels between VTE and non VTE patients, while significantly higher levels of LDH (p = 0.04) and IL-6 (p = 0.04) were observed in VTE patients in comparison to non-VTE patients. In conclusion, our findings showed a quite high prevalence of VTE in COVID-19 patients. Raised inflammatory indexes and increased serum levels of pro-inflammatory cytokines should raise the clinical suspicion of VTE.
Highlights
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is responsible for acute respiratory distress syndrome1 3 Vol.:(0123456789)Internal and Emergency Medicine (2021) 16:1141–1152 in a significant proportion of affected patients (27–31%) [1, 2].The clinical spectrum of SARS-CoV-2 infection appears to be wide, encompassing asymptomatic infection, mild flulike syndrome, and severe viral pneumonia with respiratory failure and superimposed bacterial infections which may be fatal [3,4,5].Venous thromboembolism (VTE) includes deep vein thrombosis (DVT), pulmonary embolism (PE) and portal vein thrombosis
In previous Asian series, thromboembolic events have been reported in roughly one fourth of COVID-19 patients admitted to the intensive care unit, and these findings correlated with a poor prognosis [7]
We examined the correlation between DVT and selected inflammatory markers, including C-reactive protein (CRP), interleukin (IL)-6, mean platelet volume (MPV), neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR)
Summary
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is responsible for acute respiratory distress syndrome1 3 Vol.:(0123456789)Internal and Emergency Medicine (2021) 16:1141–1152 in a significant proportion of affected patients (27–31%) [1, 2].The clinical spectrum of SARS-CoV-2 infection appears to be wide, encompassing asymptomatic infection, mild flulike syndrome, and severe viral pneumonia with respiratory failure and superimposed bacterial infections which may be fatal [3,4,5].Venous thromboembolism (VTE) includes deep vein thrombosis (DVT), pulmonary embolism (PE) and portal vein thrombosis. Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is responsible for acute respiratory distress syndrome. The association between VTE and COVID-19 was described for the first time by Zhou et al [6], who identified thrombotic events in 2.9% of a cohort of COVID-19 patients. In previous Asian series, thromboembolic events have been reported in roughly one fourth of COVID-19 patients admitted to the intensive care unit, and these findings correlated with a poor prognosis [7]. A number of pathogenic mechanisms have been hypothesized for VTE in COVID-19 patients, including active inflammation, immobilization and intensive care treatments, but the limited evidence available in the literature does not allow to estimate the relative contribution of each of the abovementioned factors [8]
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