Disseminated Intravascular Coagulation (DIC)

  • Disseminated Intravascular Coagulation (DIC) represents an end-stage systemic state of global hemostatic dysfunction occurring secondary to a wide variety of insults. DIC is characterized by wide-spread inappropriate activation of both platelets aggregation and coagulation within the microcirculation, yielding the generation of micro-thrombi throughout the micro-vasculature. Ironically, DIC can result in rapid consumption of platelets and coagulation factors, yielding insufficient hemostasis and thus bleeding in other parts of the vasculature.
  • Overview
    • DIC can be thought of as a final, common result of a variety of etiologies that initiate systemic inappropriate activation of hemostasis. These etiologies can be divided into two basic categories: 1) Those that release systemic levels of thrombogenic substances, 2) Those that yield systemic damage to microvascular endothelium.
  • Systemic Release of Thrombogens
    • Sepsis: Sepsis likely represents the most common cause of DIC clinically. Overwhelming presence of bacteria and their toxins likely result in systemic release of thrombogens from immune cells. In certain cases such as Neisseria meningitides, bacterial toxins may activate the coagulation cascade directly.
    • Obstetrical Complications: Fetal components can be highly thrombogenic if released into the maternal circulation and thus DIC is a common result of placental abruption, amniotic fluid embolism, or retention of dead fetal components
    • Neoplasms: Certain neoplasms appear to secrete factors which activate the coagulation cascade. The most dramatic example is the promyelocytic subtype of Acute Myeloid Leukemia in which extruded granules can directly activate coagulation.
  • Systemic Microvascular Damage
    • Endothelial damage is a key trigger of hemostasis and it is unsurprising that systemic injury to the endothelium would result in systemic activation of hemostasis. Widespread trauma and burns often initiate DIC. Furthermore, sepsis can also lead to global microvascular damage.
Pathogenesis and Clinical Consequences
  • Overview
    • Whatever the triggering mechanism, widespread activation of hemostasis within the microcirculation leads to two basic consequences: 1) Generation of widespread micro-thrombi, and 2) Consumption of coagulation factors.
  • Widespread Micro-thrombi Formation
    • Thrombi typically form in the small vessels such as arterioles and capillaries of multiple organs. Naturally, these micro-thrombi can block downstream blood flow and thus cause micro-infarctions throughout the body.
    • When micro-thrombi partially block blood flow, red blood cells can be physically sheared as they move past, resulting in an intravascular hemolytic anemia akin to a Microangiopathic Hemolytic Anemia (MAHA).
  • Consumptive Coagulopathy
    • DIC can rapidly deplete the circulating reserves of platelets and coagulation factors within hours to days. Additionally, activation of the coagulation cascade yields release of a variety of coagulation inhibitors. Normally these serve to limit extension of a clot (See Coagulation); however, in the pathological context of DIC they can spread systemically to prevent clot formation. Together, these processes yield a significant bleeding disorder and patients with DIC can tragically suffer from extensive hemorrhagic complications.
Laboratory Features
  • It is important to be able to distinguish the presence of DIC from other hemostatic disorders and a few key laboratory features should be appreciated. Because DIC results in consumption platelets as well as all the coagulation factors, it is the only hemostatic disorder that yields defects in all laboratory indices of hemostasis. It is characterized by thrombocytopenia along with increases in both PT and PTT. Because of widespread consumption of fibrinogen and the subsequent generation of fibrin split products, DIC is also characterized by reduced fibrinogen] levels and increased D-dimer levels.