COVID-19 and its implications for thrombosis and anticoagulation

Abstract

Severe acute respiratory syndrome coronavirus 2, coronavirus disease 2019 (COVID-19)-induced infection can be associated with a coagulopathy, findings consistent with infection-induced inflammatory changes as observed in patients with disseminated intravascular coagulopathy (DIC). The lack of prior immunity to COVID-19 has resulted in large numbers of infected patients across the globe and uncertainty regarding management of the complications that arise in the course of this viral illness. The lungs are the target organ for COVID-19; patients develop acute lung injury that can progress to respiratory failure, although multiorgan failure can also occur. The initial coagulopathy of COVID-19 presents with prominent elevation of D-dimer and fibrin/fibrinogen-degradation products, whereas abnormalities in prothrombin time, partial thromboplastin time, and platelet counts are relatively uncommon in initial presentations. Coagulation test screening, including the measurement of D-dimer and fibrinogen levels, is suggested. 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. Although D-dimer, sepsis physiology, and consumptive coagulopathy are indicators of mortality, current data do not suggest the use of full-intensity anticoagulation doses unless otherwise clinically indicated. Even though there is an associated coagulopathy with COVID-19, bleeding manifestations, even in those with DIC, have not been reported. If bleeding does occur, standard guidelines for the management of DIC and bleeding should be followed.

Predictors of mortality in patients with coronavirus disease 2019: a systematic review and meta-analysis

“…These ndings indicated that excessive activation of the coagulation cascade and PLTs existed in the progression of COVID-19 infection. The underlying mechanisms of activated coagulation remain unclear but may be due to in ammatory responses induced by SARS-CoV-2 [61]. Coagulation screening, especially the determination of D-dimer and PLT levels, has been suggested.…”

The Emerging Role of Neutrophil Extracellular Traps in Severe Acute Respiratory Syndrome Coronavirus 2 (COVID-19)

“…The disease has been revealed as a systemic disease, the increased expression of ACE2 in patients with comorbidities may represent a propensity for an increased viral load of infection and the spread of the virus to extrapulmonary tissues (4,5). This systemic virus dissemination brings complications to different organs of the body in patients who evolve for the severe clinical form, which may affect central nervous system, eyes, heart and gut, leading to multi-organ dysfunction and extensive microthrombus formation with multiorgan failure (6). Evidences have shown that patients recovering from COVID-19 infection show signs of antiviral T and B cellmediated adaptive immunity and memory, with clonal expansion and activation (7).…”

Haematological factors of SARS-CoV-2 infection aggravation: a COVID'HEMOS study

“…The prevalence of pulmonary embolism in the ICU is near 20% (40). ISTH and the American Society of Hematology recommended prophylactic dose of low molecular weight heparin to prevent thrombotic event (47)(48)(49). Even with thromboprophylaxis, 7.7% of patients in academic hospital of Milan developed thrombotic event (50).…”