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Hematological Phenotype of COVID-19-Induced Coagulopathy: Far from Typical Sepsis-Induced Coagulopathy

Yutaka Umemura1,2, Kazuma Yamakawa3, Takeyuki Kiguchi1

  • 1Division of Trauma and Surgical Critical Care, Osaka General Medical Center, 3-1-56 Bandai-Higashi, Sumiyoshi, Osaka 558-8558, Japan.

Journal of Clinical Medicine
|September 9, 2020
PubMed

Insights

Severe COVID-19 coagulopathy differs from sepsis. COVID-19 patients show milder changes in platelet counts and coagulation times but higher D-dimer levels, suggesting localized clotting rather than systemic hypercoagulation.

Area of Science:

  • Hematology
  • Infectious Diseases
  • Critical Care Medicine

Background:

  • Blood coagulation disorders are common in severe COVID-19.
  • Distinguishing COVID-19 coagulopathy from sepsis-induced coagulopathy (SIC) is crucial due to limited evidence.

Purpose of the Study:

  • To elucidate the specific pattern of coagulopathy in COVID-19 pneumonia.
  • To compare hemostatic biomarkers between COVID-19-induced ARDS and non-COVID-19-induced septic ARDS.

Main Methods:

  • Retrospective, observational study of adult patients with COVID-19-induced ARDS.
  • Comparison of hemostatic biomarkers with non-COVID-19-induced septic ARDS.
  • Multilevel mixed-effects regression analysis and Kaplan-Meier survival analysis.

Main Results:

  • COVID-19 patients (n=24) showed milder alterations in platelet count, antithrombin activity, and prothrombin time compared to non-COVID-19 ARDS patients (n=200).
  • Significantly higher fibrin/fibrinogen degradation product and D-dimer levels were observed in the COVID-19 group.
  • COVID-19 patients exhibited elevated thrombin-antithrombin and plasmin-alpha2-plasmin inhibitor complexes with normal plasminogen activator inhibitor-1 levels.

Conclusions:

  • COVID-19-induced coagulopathy presents a distinct hematological phenotype compared to typical SIC.
  • Severe COVID-19 may promote local thrombus formation rather than systemic hypercoagulation and suppressed fibrinolysis.
Abstract

Keywords:
COVID-19acute respiratory distress syndromebiomarkersblood coagulation disorderssepsis

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