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Pulmonary thrombosis in Covid-19: before, during and after hospital admission.

ABSTRACT: Disordered coagulation, endothelial dysfunction, dehydration and immobility contribute to a substantially elevated risk of deep venous thrombosis, pulmonary embolism (PE) and systemic thrombosis in coronavirus disease 2019 (Covid-19). We evaluated the prevalence of pulmonary thrombosis and reported RV (right ventricular) dilatation/dysfunction associated with Covid-19 in a tertiary referral Covid-19 centre. Of 370 patients, positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), 39 patients (mean age 62.3?±?15 years, 56% male) underwent computed tomography pulmonary angiography (CTPA), due to increasing oxygen requirements or refractory hypoxia, not improving on oxygen, very elevated D-dimer or tachycardia disproportionate to clinical condition. Thrombosis in the pulmonary vasculature was found in 18 (46.2%) patients. However, pulmonary thrombosis did not predict survival (46.2% survivors vs 41.7% non-survivors, p?=?0.796), but RV dilatation was less frequent among survivors (11.5% survivors vs 58.3% non-survivors, p?=?0.002). Over the following month, we observed four Covid-19 patients, who were admitted with high and intermediate-high risk PE, and we treated them with UACTD (ultrasound-assisted catheter-directed thrombolysis), and four further patients, who were admitted with PE up to 4 weeks after recovery from Covid-19. Finally, we observed a case of RV dysfunction and pre-capillary pulmonary hypertension, associated with Covid-19 extensive lung disease. We demonstrated that pulmonary thrombosis is common in association with Covid-19. Also, the thrombotic risk in the pulmonary vasculature is present before and during hospital admission, and continues at least up to four weeks after discharge, and we present UACTD for high and intermediate-high risk PE management in Covid-19 patients.

SUBMITTER: Vlachou M

PROVIDER: S-EPMC7775738 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Pulmonary thrombosis in Covid-19: before, during and after hospital admission.

Vlachou Maria M Drebes Anja A Candilio Luciano L Weeraman Deshan D Mir Naheed N Murch Nick N Davies Neil N Coghlan J Gerry JG

Journal of thrombosis and thrombolysis 20210101 4

Disordered coagulation, endothelial dysfunction, dehydration and immobility contribute to a substantially elevated risk of deep venous thrombosis, pulmonary embolism (PE) and systemic thrombosis in coronavirus disease 2019 (Covid-19). We evaluated the prevalence of pulmonary thrombosis and reported RV (right ventricular) dilatation/dysfunction associated with Covid-19 in a tertiary referral Covid-19 centre. Of 370 patients, positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 ...[more]

PMID: 33386559

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Project description:Introduction: COVID-19 has had a huge impact on society and healthcare and it has been suggested that people with periodontal disease are at risk of having worse outcomes from the disease. The aim of this study was to quantify the impact of periodontal disease on hospital admission and mortality during the COVID-19 pandemic. Materials and Methods: The study extracted UK Biobank participants who had taken a COVID-19 test between March and June 2020 (n = 13,253), of which 1,616 were COVID-19 positive (12%) and 11,637 were COVID-19 negative (88%). Self-reported oral health indicators of painful or bleeding gums and loose teeth were used as surrogates for periodontal disease, participants who did not report any of the aforementioned indicators were used as controls. Multivariable logistic regressions were used to obtain crude and adjusted odds ratios of COVID-19 infection, subsequent hospital admission and mortality adjusted for demographics, BMI, biomarkers, lifestyle and co-morbidities. Results: Painful gums, bleeding gums and loose teeth were reported in 2.7, 11.2 and 3.3% of participants with COVID-19 infection, respectively. Risk of COVID-19 infection in participants with painful or bleeding gums and loose teeth compared to controls was not increased (odds ratio [OR]: 1.10, 95% CI: 0.72-1.69; OR: 1.15, 95% CI: 0.84-1.59). COVID-19 positive participants with painful or bleeding gums had a higher risk of mortality (OR: 1.71, 95% CI: 1.05-2.72) but not hospital admission (OR: 0.90, 95% CI: 0.59-1.37). Participants with loose teeth did not show higher risk of hospital admission or mortality compared to the control group (OR = 1.55, 95% CI: 0.87-2.77; OR: 1.85; 95% CI: 0.92-2.72). Conclusion: There was insufficient evidence to link periodontal disease with an increased risk of COVID-19 infection. However, amongst the COVID-19 positive, there was significantly higher mortality for participants with periodontal disease. Utilization of linked dental and hospital patient records would improve the understanding of the impact of periodontal disease on COVID-19 related outcomes.

Project description:BackgroundProgressive respiratory failure is the primary cause of death in the coronavirus disease 2019 (Covid-19) pandemic. Despite widespread interest in the pathophysiology of the disease, relatively little is known about the associated morphologic and molecular changes in the peripheral lung of patients who die from Covid-19.MethodsWe examined 7 lungs obtained during autopsy from patients who died from Covid-19 and compared them with 7 lungs obtained during autopsy from patients who died from acute respiratory distress syndrome (ARDS) secondary to influenza A(H1N1) infection and 10 age-matched, uninfected control lungs. The lungs were studied with the use of seven-color immunohistochemical analysis, micro-computed tomographic imaging, scanning electron microscopy, corrosion casting, and direct multiplexed measurement of gene expression.ResultsIn patients who died from Covid-19-associated or influenza-associated respiratory failure, the histologic pattern in the peripheral lung was diffuse alveolar damage with perivascular T-cell infiltration. The lungs from patients with Covid-19 also showed distinctive vascular features, consisting of severe endothelial injury associated with the presence of intracellular virus and disrupted cell membranes. Histologic analysis of pulmonary vessels in patients with Covid-19 showed widespread thrombosis with microangiopathy. Alveolar capillary microthrombi were 9 times as prevalent in patients with Covid-19 as in patients with influenza (P<0.001). In lungs from patients with Covid-19, the amount of new vessel growth - predominantly through a mechanism of intussusceptive angiogenesis - was 2.7 times as high as that in the lungs from patients with influenza (P<0.001).ConclusionsIn our small series, vascular angiogenesis distinguished the pulmonary pathobiology of Covid-19 from that of equally severe influenza virus infection. The universality and clinical implications of our observations require further research to define. (Funded by the National Institutes of Health and others.).

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Pulmonary thrombosis in Covid-19: before, during and after hospital admission.

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Pulmonary thrombosis in Covid-19: before, during and after hospital admission.

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