Pulmonary embolism and screening for concomitant proximal deep vein thrombosis in noncritically ill hospitalized patient
- PDF / 385,071 Bytes
- 3 Pages / 595.276 x 790.866 pts Page_size
- 114 Downloads / 199 Views
CE - COMMENTARY
Pulmonary embolism and screening for concomitant proximal deep vein thrombosis in noncritically ill hospitalized patients with coronavirus disease 2019 Chiara Lazzeri1 · Manuela Bonizzoli1 · Andrea Franci1 · Filippo Socci1 · Adriano Peris1 Received: 14 July 2020 / Accepted: 22 July 2020 © Società Italiana di Medicina Interna (SIMI) 2020
Alterations in the coagulation system related to COVID infection still represents a challenge for clinicians in every day practice despite the growing number of investigations on this topic, and some issues (i.e., timing and doses of anticoagulants, risk stratification of the hemorrhagic/thrombotic risk in each patient) remain to date to be completely understood [4–6]. Coagulation disorders are not peculiar to COVID disease since thrombotic complications and hematologic manifestations (in primis thrombocytopenia) were reported also in SARS-CoV-1 and MERS-CoV disease [7], though the latter viral diseases have been less extensively investigated. In COVID infection, alterations in the coagulation system are detectable in all patients, independently of disease severity which itself does influence the degree and extension of coagulation disorders, particularly thrombotic events. This is why every physician in charge of a COVID patient has to assess, on admission and serially on hospital course, the functional state/alterations of the coagulation system and eventually to rule out thrombotic events by screening ultrasound. Pulmonary embolism has been described as a frequent thrombotic event, often in the absence of detectable deep venous thrombosis (DVT) [1], suggesting pulmonary thrombosis, secondary to vascular damage, rather than embolism [8]. This arises questions, so far not answered, on the most efficacious antithrombotic treatment in these patients and, more importantly, on the role of pulmonary thrombosis/embolism in causing acute respiratory failure or just contributing to it. COVID infection attacks the coagulation system mainly through an immuno-triggered thrombo-inflammation supported by both an endotheliopathy and a hypercoagulability * Chiara Lazzeri [email protected] 1
Intensive Care Unit and Regional ECMO Referral Centre, Azienda Ospedaliero-Universitaria Careggi, Largo Brambilla 3, 50134 Florence, Italy
state. The endothelium seems to play a pivotal role in inducing the procoagulant state since COVID-19-related proinflammatory cytokines induce an endothelial injury resulting in the release of ultralarge von Willebrand factor multimers (ULVWF) involved in primary hemostasis and the overexpression of tissue factor [7,9,10]. No patient is spared. The phenomenon may be aggravated by other clinical factors including hypoxemia (secondary to ARDS), hyperthermia (with activation of platelets and coagulation), and/or hypovolemia (mainly secondary to diarrhea). The more severe the COVID disease the more prominent coagulation disorders. Hypoxemia (secondary to ARDS) may also shift the basal antithrombotic and antiinflammatory phenotype of the endothelium to
Data Loading...
