Disseminated Intravascular Coagulation (DIC) as a Predecessor of Thromboinflammation and Multiorgan Organ Failure in a Patient with Coronavirus Disease 2019 (COVID-19), A Case Report

Introduction: Individuals with COVID-19 may have complex coagulation abnormalities in consistence with hypercoagulability. This manifests as high plasma level of certain coagulation factors, particularly fibrinogen. DIC, on the other hand, is characterized by consumption of these factors. We present a case of COVID-19 respiratory failure at which a DIC phase was followed by thromboinflammation and organ failure. Case Presentation: A 51-year-old male presented with 3-day duration of fever and dyspnea. He had laboratoryconfirmed COVID-19 infection a day prior to his presentation. He displayed significant hypoxia and respiratory distress which led to mechanical ventilation at 48 hours post presentation. His laboratory evaluation showed a platelet count of 45 x 1000/ mm3, International Normalized Ratio (INR) of 3.2, activated Partial Thromboplastin Time of 39 seconds, Fibrinogen of 30 mg/dl, D-Dimer of <4 mcg/ml and Fibrin Split Products of 320 unigram/ml. Peripheral blood smear showed schistocytes and ultrasound of the lower extremities showed bilateral deep venous thrombosis. Thrombotic thrombocytopenic purpura (TTP) and Disseminated Intravascular Coagulation (DIC) were considered. Serum Disintegrin And Metalloprotease with a ThromboSpondin type 1 motif, member 13 (ADAMTS-13) level was ordered, plasmapheresis trial initiated and IV argatroban drip started. Platelet count normalized with 48 hours. ADAMTS-13 level was inconsistent with TTP. On the sixth day of admission, serum fibrinogen level increased to 457 mg/dl which coexisted with worsening ventilatory requirements. A similar pattern of increasing serum D-Dimer level, ferritin and creatinine was observed together with the development of shock and multiorgan failure syndrome. Patient eventually succumbed to his critical illness on the 28th day of admission. Discussion: Endothelial injury [1] and hypercoagulable status [2] cause COVID Coagulopathy. DIC is predominately a consumptive disorder associated with bleeding, COVID- associated coagulopathy is associated with increasing thrombosis. In s series that reported on thromboembolic events, none of the patients developed overt DIC[3]. While thromboembolic events in COVID-19 are associated with increased mortality, the clinical significance of this compensated form of DIC is unknown. Conclusion:Critically ill patients with COVID-19 may display “compensated” DIC. Whether this is a separate entity or lies within a large spectrum of different coagulation abnormalities is unknown. The clinical significance of it is unknown wither. Randomized clinical trials are needed for further understanding.