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How does disseminated intravascular coagulation lead to severe bleeding?

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blood disease Peripheral blood smear revealing histopathologic features indicative of a blast crisis in a case of chronic myelogenous leukemia (CML). Blast crisis occurs when one-fifth to one-third of the cells in the blood or bone marrow are immature blood cells, or blast cells. This phase of CML is characterized by fever, weakness, and an enlarged spleen.

Disseminated intravascular coagulation (DIC) leads to severe bleeding through a paradoxical process of systemic over-activation followed by depletion of clotting resources.1

In this condition, the body’s coagulation system is triggered inappropriately by underlying factors such as severe tissue injury, infections, or certain cancers. This activation causes the widespread formation of microvascular clots throughout the body, which consumes platelets and essential coagulation factors at an accelerated rate.1

As these vital components are exhausted, the blood loses its ability to form necessary clots at sites of injury, resulting in a severe bleeding disorder. Furthermore, the body’s fibrinolytic system—which is responsible for dissolving clots—is simultaneously activated. This leads to the destruction of both fibrinogen and existing fibrin clots, further exacerbating the inability to maintain hemostasis and contributing to life-threatening hemorrhage. Treatment focuses on addressing the primary cause that triggered this systemic activation.1