Figure 2.

Pathophysiology of a Cytokine Storm

An infectious or non-infectious stimulus in barrier sites such as the gut or lungs that leads to tissue damage initiates a complex series of events. In circumstances that leads to vascular damage, the coagulation system is critical for tissue repair, but this can progress to the development of DIC. The early response to microbial invasion or tissue damage is characterized by the innate production of cytokines and the induction of emergency granulopoiesis that leads to the mobilization of neutrophils and monocytes. These events will engage and amplify NK and T cell production of proinflammatory cytokines. These can promote capillary leak syndrome and thrombus formation that can progress to DIC. High circulating levels of these cytokines can cause cell death and tissue damage, while their ability to activate macrophages can lead to erythro-phagocytosis and anemia. The combination of anemia, alterations in vascular hemostasis, and cytokine-mediated damage can result in multi-organ failure.