Thrombotic events are common complications in COVID-19 patients that include both thrombus formation in large vessels and the microvasculature of the lung and other organs. COVID-19-associated coagulopathy (CAC) and disseminated intravascular coagulation (DIC) have similarities and differences, and whether CAC is a form of DIC is the subject of debate. Reported mechanisms of CAC include activated coagulation, endotheliopathy, up-regulated innate and adaptive immunity, and activated complement system. Although the clinical features and laboratory findings of CAC and DIC seem different, there are fundamental similarities that should be considered. Basically, the pathological findings of COVID-19 fall within the scope of the definition of DIC, i.e., systemic activation of coagulation caused by or resulting from the microvascular damage. Therefore, we suggest that although CAC differs from usual infection-associated DIC, its various features indicate that it can be considered a thrombotic phenotype DIC. This review summarizes the current knowledge about CAC including differences and similarities with sepsis-associated DIC.