Organ Dysfunction in Sepsis-associated Intravascular Coagulation

Abstract

Sepsis is frequently associated with disseminated intravascular coagulation (DIC) and multiple organ damage. It is widely accepted that DIC is not merely a complication but also plays a role in the development of organ dysfunction. Thrombus formation in the microvasculature leads to impaired tissue perfusion and organ damage. Activated neutrophils interacting with platelets, endothelial injury, and an imbalance of coagulation and fibrinolysis are the essence of thromboinflammation induced in sepsis-associated DIC. The above mechanisms are typically seen in sepsis-associated acute kidney injury (AKI), and the development of AKI is known to be strongly associated with the severity of sepsis. It is important to recognize the pathway of this mechanism in the context of sepsis management.

Keywords: acute kidney injury; disseminated intravascular coagulation; neutrophil; sepsis; thrombus.

Figure 1

Pathologic findings of the kidney Sepsis-associated disseminated intravascular coagulation (DIC) was induced by intravenous infusion of E. coli. Rats were sacrificed 2.5 hours after the infusion, and kidney specimens were stained with hematoxylin and eosin. In the normal kidney (left), red cells and the capillary lumen were observed. In contrast, in the kidney of a septic DIC rat, the glomerular capillary was occupied by leukocytes (arrows), and the capillary lumen was hardly visible (right). Mild renal tubular cell injury was observed in the septic DIC rat.