Related Experiment Video
Updated: Nov 17, 2025

Author Spotlight: Deciphering Coagulation Disorders in Traumatic Brain Injury Patients
Published on: August 4, 2023
No Evidence for Classic Thrombotic Microangiopathy in COVID-19
Tanja Falter1, Heidi Rossmann1, Philipp Menge2
1Institute of Clinical Chemistry and Laboratory medicine, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.
Insights
Disseminated intravascular coagulation (DIC) occurred in some COVID-19 patients, but fibrinogen and platelet consumption were mostly compensated. Thrombotic microangiopathy (TMA) hallmarks were absent, suggesting localized alveolar microcirculation issues.
Area of Science:
- Hematology
- Infectious Diseases
- Critical Care Medicine
Background:
- Coronavirus disease-2019 (COVID-19) is a systemic infection impacting the respiratory tract.
- Some patients develop hemostatic abnormalities, increasing mortality risk.
Purpose of the Study:
- To investigate the occurrence and characteristics of disseminated intravascular coagulation (DIC) and thrombotic microangiopathy (TMA) in COVID-19 patients.
- To analyze laboratory parameters and clinical features associated with these hemostatic disorders in COVID-19.
Main Methods:
- Retrospective analysis of 65 COVID-19 patients (SARS-CoV-2 infection) from March to May 2020.
- Assessment of disseminated intravascular coagulation (DIC) and thrombotic microangiopathy (TMA) using ISTH criteria and laboratory data.
- Analysis of fibrinogen levels, platelet counts, and ADAMTS13 activity.
Main Results:
- Seven out of 65 COVID-19 patients (10.8%) showed overt DIC.
- Fibrinogen levels dropped significantly in DIC patients but remained above 100 mg/dl.
- Hallmarks of TMA, including thrombocytopenia and microangiopathic hemolytic anemia, were absent. ADAMTS13 activity was mildly reduced in some patients with elevated procalcitonin.
Conclusions:
- DIC occurred in a subset of COVID-19 patients, but consumption of fibrinogen and platelets was largely compensated.
- Classic TMA and TTP were excluded by ADAMTS13 assays and absence of key TMA markers.
- A hypothesis suggests COVID-19-associated microangiopathy is localized to alveolar microcirculation, explaining limited erythrocyte fragmentation and platelet consumption.
Background:
Coronavirus disease-2019 (COVID-19) triggers systemic infection with involvement of the respiratory tract. There are some patients developing haemostatic abnormalities during their infection with a considerably increased risk of death.
Materials And Methods:
Patients (n = 85) with SARS-CoV-2 infection attending the University Medical Center, Mainz, from 3 March to 15 May 2020 were retrospectively included in this study. Data regarding demography, clinical features, treatment and laboratory parameters were analyzed. Twenty patients were excluded for assessment of disseminated intravascular coagulation (DIC) and thrombotic microangiopathy (TMA) due to lack of laboratory data.
Results:
COVID-19 patients (n = 65) were investigated, 19 with uncomplicated, 29 with complicated, and 17 with critical course; nine (13.8%) died. Seven patients showed overt DIC according to the ISTH criteria. The fibrinogen levels dropped significantly in these patients, although not below 100 mg/dl. Hallmarks of TMA, such as thrombocytopenia and microangiopathic haemolytic anaemia, were not detected in any of our COVID-19 patients. ADAMTS13 activity was mildly to moderately reduced in 4/22 patients, all having strongly elevated procalcitonin levels.
Conclusion:
DIC occurred in 7/65 COVID-19 patients but fibrinogen and platelet consumption were compensated in almost all. ADAMTS13 assays excluded TTP and hallmarks of classic TMA were absent in all investigated patients. We hypothesize that the lacking erythrocyte fragmentation and only mild platelet consumption in severe COVID-19 are due to a microangiopathy predominantly localized to the alveolar microcirculation with a low blood pressure gradient.
Related Concept Videos
Venous Thrombosis II: Clinical Manifestations and Diagnostic Studies
Endocarditis II: Clinical Features of Infective Endocarditis
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests
Myocarditis II: Clinical Features and Diagnostic Tests
Venous Thrombosis I: Introduction
Anticoagulant Drugs: Low-Molecular-Weight Heparins

