ABSTRACT
Disseminated intravascular coagulation (DIC) is characterized by the in vivo activation
of the coagulation system, which results in the intravascular deposition of fibrin
and consumption bleeding. DIC is a serious hemostatic complication of trauma. It can
be clearly distinguished from physiological hemostatic response to trauma by using
sensitive coagulofibrinolytic molecular markers. Physiological hemostasis to injuries
is similar in all kinds of trauma without exception. There is an increase in circulating
proinflammatory cytokines in DIC patients after trauma. Elevated cytokines induce
tissue factor-mediated activation of coagulation, suppression of the anticoagulant
pathway, and plasminogen activator inhibitor-1 (PAI-1)-mediated inhibition of fibrinolysis
followed by disseminated fibrin deposition in the microvasculature. In addition to
the occlusive microvascular thrombosis and hypoxia, sustained systemic inflammatory
response characterized by neutrophil activation and endothelial damage plays a pivotal
role in the development of multiple organ dysfunction syndrome (MODS) in posttrauma
DIC patients. DIC associated with sustained systemic inflammatory response syndrome
(SIRS) after trauma leads to the development of MODS, which is the main determinant
of patients' outcome after trauma.
KEYWORD
Disseminated intravascular coagulation (DIC) - trauma - multiple organ dysfunction
syndrome (MODS) - systemic inflammatory response syndrome (SIRS) - inflammation
