Abnormal coagulation linked to poorer COVID-19 prognosis

Coagulation

By Nicola Garrett

6 May 2020

COVID-19 is associated with a unique yet abnormal clotting disorder which is primarily focused in the lungs and is a likely contributor to high mortality rates, new research concludes.

The study by haematologists from the Irish Centre for Vascular Biology, RCSI and St James’s hospital, Dublin, included 83 consecutive adult patients with COVID-19 seen at their centre.

While prothrombin and activated partial thromboplastin time were normal, D-dimer levels were significantly increased in 67% of the patients on admission.

Abnormal coagulation was also associated with a poorer prognosis, the researchers reported in their study published in the British Journal of Haematology.

Along with fibrinogen and CRP levels, D-dimer levels were significantly higher in the subgroup who eventually needed ICU admission (median 1003 versus 804 ng/mL; p = 0.018) but critically,  disseminated intravascular coagulopathy (DIC) was not evident.

“These data suggest that the diffuse bilateral pulmonary inflammation observed in COVID-19 is associated with a novel pulmonary-specific vasculopathy which we recently termed pulmonary intravascular coagulopathy (PIC) as distinct to DIC,” they wrote.

The authors noted that LMWH, at least in standard prophylactic doses, did not significantly impact the progressive increase in D-dimer levels seen in the patients with severe COVID-19.

“Further adequately-powered randomised controlled studies will be required to determine whether more intensive anticoagulation and/or targeted anti-inflammatory therapies may be useful in attenuating  PIC in selected patients with  severe COVID-19,” the authors wrote.

According to the authors their data supported the hypothesis that COVID-19 associated coagulopathy contributed to the underlying pulmonary pathogenesis.

“In the context of this lung-centric vasculopathy, we  hypothesise that  the refractory  ARDS phenotype  observed in severe COVID-19 is due to concurrent ‘double-hit’ pathologies targeting both ventilation (V) and perfusion  (Q)  within  the  lungs  where  alveoli  and  pulmonary microvasculature  exist in  close anatomical juxtaposition,” they concluded.

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