Disseminated
intravascular coagulation results in the formation of numerous
fibrin-rich microthrombi which are deposited in the small blood vessels
at different sites throughout the body. The kidney is one of the most
frequently affected organs.
Update December 17, 2001
 Fibrinolysis
in Disseminated Intravascular Coagulation.
Studies in experimental models for sepsis, the most common cause
of disseminated intravascular coagulation (DIC), have put forward
the concept of a procoagulant state that is characterized by thrombin
generation exceeding that of plasmin. Convincing evidence
indicates that this imbalance between coagulation and fibrinolysis
is due to increased levels of plasminogen activator inhibitor
type 1 (PAI-1). Levels of this fibrinolysis inhibitor indeed
correlate with outcome and severity of multiple organ failure in
patients with sepsis, as well as in patients with DIC from other
causes. Hence we suggest that PAI-1 constitutes an important
target for therapy in patients with DIC.
Semin
Thromb Hemost. 2001;27(6):633-638 |
|
It is the widespread deposition of fibrin
in small blood vessels that may cause tissue or organ damage from ischemia.
Depletion of clotting factors and platelets results in a bleeding diathesis.
Simultaneous activation of plasmin and resulting fibrinolysis also occurs.
Ths has been reported in association with any severe illness or may be
more insidious in certain chronic diseases. DIC is second only to liver
disease as a cause of acquired coagulopathy.
Abnormal tissue factor (TF) expression is
a major mechanism initiating DIC in many disorders. Common illness associated
with DIC include: obstetric complications; infections; neoplasms; vascular
disorders; massive injury and trauma.
Clinical picture: generalized bleeding;
thromboembolic phenomena.
Laboratory: in acute DIC usually
the prothrombin time (PT), partial thromboplastin time (PTT), and thrombin
time are prolonged. The platelet count is decreased. Fibrin degradation
products are elevated. Multiple clotting factors, expecially fibrinogen
and factors V, VIII, and XIII, are usually depressed.
Conventional treatment:
- treatment of the underlying illness -> spontaneous
reversal
- transfusion of red blood cells and platelets
Controversies:
- Fresh frozen plasma or Cryoprecipitate -> might
add "fuel to the fire"
- Heparin -> might increase the blleding tendence;
no randomized trials have shown improved outcome.
(From Hematology/Oncology Secrets,
Hanley&Belfus Inc. 1994)
Novel treatments are being investigated for
treating DIC; many of these experimental modalities target the excessive
TF activity that characterizes DIC (Am
J Hematol 1998 Sep;59(1):65-73)
Antithrombin III, antifibrinolytic agents, activated
protein C, tissue factor pathway inhibitor, hirudin, or synthetic serine
protease inhibitors. (Semin
Thromb Hemost 1998;24(1):53-9) |
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