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Acute pulmonary embolism and COVID-19 pneumonia: a random association?

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TLDR
The absence of major predisposing factors in this case of diffuse bilateral COVID-19 pneumonia seems to confirm the role of severe infections as a precipitant factor for acute venous thrombo-embolism and the causal relationship.
Abstract
In a 75-year-old Covid-19positive woman hospitalized for severe bilateral pneumonia, CT scan documented bilateral pulmonary embolism associated with extensive groundglass opacifications involving both the lung parenchymas. Acute infections are associated with a transient increased risk of venous thromboembolic events. A COVID-19positive 75-year-old woman, with severe bilateral pneumonia and concomitant acute pulmonary embolism, was hospitalized after 10 days of fever and a recent onset of dyspnoea. She was haemodynamically stable and without strong predisposing risk factors for venous thrombo-embolism. The baseline ECG was normal. A modest leucocytosis was present (11.360/mm) with increased values of C-reactive protein (180 mg/L), troponin I (3240.4 ng/mL), and D-dimer (21 lg/mL). While on oxygen, arterial blood gas revealed a PaO2 of 78.0 mmHg with a PcO2 of 25.1 mmHg and an sO2 of 95.6%. A right basal infiltrate was evident at the chest X-ray, while echocardiographic evaluation showed a dilated and severely hypokinetic right ventricle with a mean derived pulmonary arterial pressure of 60 mmHg. CT scan documented the presence of a bilateral filling defect diagnostic for pulmonary embolism (Panels 1A and B; Supplementary material online Video 1), associated with extensive ground-glass opacifications involving both the lung parenchymas with predominant consolidation in the posterior basal segment of the left lower lobe (Panels 1C and D; Supplementary material online Video 2). Lower-limb compression ultrasonography was negative. Based on these findings, treatment with low molecular weight heparin, lopinavir/ritonavir, and hydroxychloroquine was started. In conclusion, the absence of major predisposing factors in this case of diffuse bilateral COVID-19 pneumonia seems to confirm the role of severe infections as a precipitant factor for acute venous thrombo-embolism and the causal relationship.

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COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-up

Behnood Bikdeli, +50 more
TL;DR: The current understanding of the pathogenesis, epidemiology, management and outcomes of patients with COVID-19 who develop venous or arterial thrombosis, and of those with preexistingThrombotic disease who develop CO VID-19 are reviewed.
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Factors associated with hospital admission and critical illness among 5279 people with coronavirus disease 2019 in New York City: prospective cohort study.

TL;DR: Age and comorbidities were found to be strong predictors of hospital admission and to a lesser extent of critical illness and mortality in people with coronavirus disease 2019 in the United States; however, impairment of oxygen on admission and markers of inflammation were most strongly associated with critical illnesses and mortality.
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COVID-19 and its implications for thrombosis and anticoagulation.

TL;DR: COVID-19–associated coagulopathy should be managed as it would be for any critically ill patient, following the established practice of using thromboembolic prophylaxis for critically ill hospitalized patients, and standard supportive care measures for those with sepsis-induced coagULopathy or DIC.
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Cardiovascular complications in COVID-19.

TL;DR: Emergency clinicians should be aware of these cardiovascular complications when evaluating and managing the patient with COVID-19 and current therapies for CO VID-19 may interact with cardiovascular medications.
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