Abstract
The 2019 coronavirus disease (COVID-19) presents with a large variety of
clinical manifestations ranging from asymptomatic carrier state to
severe respiratory distress, multiple organ dysfunction and death. While
it was initially considered primarily a respiratory illness, rapidly
accumulating data suggests that COVID-19 results in a unique, profoundly
prothrombotic milieu leading to both arterial and venous thrombosis.
Consistently, elevated D-dimer level has emerged as an independent risk
factor for poor outcomes, including death. The pathophysiology
underlying the hyper-coagulation state is poorly understood. However, a
growing body of data suggests that the initial events occur in the lung.
A severe inflammatory response, originating in the alveoli, triggers a
dysfunctional cascade of inflammatory thrombosis in the pulmonary
vasculature, leading to a state of local coagulopathy. This is followed
by a generalized hyper-coagulation state that results in and
microvascular thrombosis. Of concern, is the observation that
anticoagulation may be inadequate in many circumstances, highlighting
the need for alternative or additional therapies. Numerous ongoing
studies investigating the pathophysiology of the COVID-19 associated
coagulopathy may provide mechanistic insights that can direct
appropriate interventional strategies.