Semin Thromb Hemost 2020; 46(07): 777-780
DOI: 10.1055/s-0040-1712155
Commentary

SARS-2 Coronavirus–Associated Hemostatic Lung Abnormality in COVID-19: Is It Pulmonary Thrombosis or Pulmonary Embolism?

Jecko Thachil
1   Department of Haematology, Manchester University Hospitals, Manchester, United Kingdom
,
Alok Srivastava
2   Department of Haematology, Christian Medical College, Vellore, India
› Author Affiliations

The coronavirus disease 2019 (COVID-19) pandemic has claimed several thousand lives since the first case was described in Wuhan, China, in December 2019.[1] This has mainly been related to pulmonary complications presumed to be due to infection-associated inflammation and the resulting cytokine storm.[2] Abnormal hemostasis was recognized early in the profile of these patients, with raised D-dimer being the most frequent abnormality in more than 70% of admitted patients with remarkably minimal changes in the remaining commonly measured hemostasis parameters (e.g., minimal prolongation of prothrombin time [PT] in some patients, and mild reduction in platelet count [almost all above 100 × 109/L] but with markedly raised fibrinogen levels and no schistocytes[3]). As may be anticipated from these laboratory findings, bleeding has not been a notable feature of this illness. In early reports, these changes were considered consistent with disseminated intravascular coagulation (DIC) or sepsis-induced coagulopathy (SIC).[3] [4] There is increasing recognition that the COVID-19-associated hemostasis abnormality (CAHA) may instead be resulting in localized thrombosis in the lungs, which has been reinforced by the fact that timely anticoagulation can be successful in reducing mortality of seriously unwell patients.[4] [5] This has led to recommendations for early intensive anticoagulation, in the absence of absolute contraindications, for all COVID-19 patients requiring hospitalization.[6] Very recent postmortem reports have in fact confirmed this hypercoagulable state, with evidence of pulmonary thrombi, mostly microvascular, in all the four decedents evaluated.[7] Recognizing the basis of the predominant lung pathology linked with the rapid clinical deterioration that is often unresponsive to ventilatory assistance and supportive care is critical to devising the interventions aimed at reducing mortality in these patients.



Publication History

Article published online:
12 May 2020

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