Disseminated intravascular coagulation (DIC) is an acquired clinicobiological
syndrome characterized by widespread activation of coagulation leading to fibrin
deposition in the vasculature, organ dysfunction, consumption of clotting
factors and platelets, and life-threatening hemorrhage. Disseminated
intravascular coagulation is provoked by several underlying disorders (sepsis,
cancer, trauma, and pregnancy complicated with eclampsia or other calamities).
Treatment of the underlying disease and elimination of the trigger mechanism are
the cornerstone therapeutic approaches. Therapeutic strategies specific for DIC
aim to control activation of blood coagulation and bleeding risk. The clinical
trials using DIC as entry criterion are limited. Large randomized, phase III
clinical trials have investigated the efficacy of antithrombin (AT), activated
protein C (APC), tissue factor pathway inhibitor (TFPI), and thrombomodulin (TM)
in patients with sepsis, but the diagnosis of DIC was not part of the inclusion
criteria. Treatment with APC reduced 28-day mortality of patients with severe
sepsis, including patients retrospectively assigned to a subgroup with
sepsis-associated DIC. Treatment with APC did not have any positive effects in
other patient groups. The APC treatment increased the bleeding risk in patients
with sepsis, which led to the withdrawal of this drug from the market. Treatment
with AT failed to reduce 28-day mortality in patients with severe sepsis, but a
retrospective subgroup analysis suggested possible efficacy in patients with
DIC. Clinical studies with recombinant TFPI or TM have been carried out showing
promising results. The efficacy and safety of other anticoagulants (ie,
unfractionated heparin, low-molecular-weight heparin) or transfusion of platelet
concentrates or clotting factor concentrates have not been objectively
assessed.