Hemostatic Abnormalities in COVID-19: An Update

  • PDF / 1,205,034 Bytes
  • 11 Pages / 595.276 x 790.866 pts Page_size
  • 11 Downloads / 237 Views

DOWNLOAD

REPORT


REVIEW ARTICLE

Hemostatic Abnormalities in COVID-19: An Update Mukul Aggarwal1 • Jasmita Dass1



Manoranjan Mahapatra1

Received: 23 May 2020 / Accepted: 3 August 2020  Indian Society of Hematology and Blood Transfusion 2020

Abstract COVID-19 has emerged as a pandemic with lung being the primarily afflicted organ. Deranged hemostasis has been observed in patients with COVID-19 with scales tipped towards a prothrombotic state. The pathogenesis differs from disseminated intravascular coagulation with a primary pulmonary localization. This is referred to as pulmonary intravascular coagulopathy with strong component of thrombo-inflammation. This is reflected in the lab tests with an increase in D-dimer which correlates with severity and outcomes of disease. Common coagulation tests such as prothrombin time, activated partial thromboplastin time are only mildly prolonged while most patients have normal to increased fibrinogen and marginal thrombocytopenia. Overall, the patients have an increase in venous and arterial thrombotic events especially in ICU patients. Routine thromboprophylaxis with low molecular weight heparin is recommended in all hospitalized patients to reduce the incidence of thrombosis. Bleeding is uncommon and treated with blood products transfusion. This review shall discuss the hemostatic abnormalities in COVID-19 patients and their impact on prognosis. In addition, strategy of thromboprophylaxis and various academic society guidelines are discussed in detail.

& Jasmita Dass [email protected] Mukul Aggarwal [email protected] Manoranjan Mahapatra [email protected] 1

Department of Hematology, All India Institute of Medical Sciences, New Delhi, New Delhi, India

Keywords COVID-19  COVID associated coagulopathy  D-dimer  Thrombosis  Pulmonary intravascular coagulopathy

Introduction COVID-19, the novel coronavirus infection started from Wuhan, China in December 2019. The outbreak was declared a public health emergency of international Concern on 30 January 2020 and later a pandemic on March 11, 2020 by World Health Organization (WHO) [1]. It is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This virus belongs to the bCoronavirus family and is partially like the SRS-CoV and MERS-CoV coronaviruses which have caused previous epidemics in China and Middle East respectively [2]. The management of the disease is challenging as the virus is highly infectious and there is a large burden of asymptomatic patients, absence of proven antiviral drugs, and limited understanding of potential benefits from antiviral antibodies [3]. Severe Acute Respiratory Distress Syndrome (ARDS), in addition progression to multi-organ dysfunction syndrome has been recognized as cause of death in most of the patients. ARDS is common amongst patients needing hospitalization, which comprise around 20% of all infected patients [4]. The exact mechanism of pulmonary complications and ARDS of COVID-19 has not been elucidated but there is a clear component of thrombo-inflammation and cytokine