Disseminated intravascular coagulation
Disseminated intravascular coagulopathy (from Latin: disseminated " scattered ", intravascularly " in vessel " coagulation " coagulation " ), short DIC (as abbreviation of disseminated intravascular coagulation ), also known as disseminated intravascular coagulation, is an acquired life-threatening condition, in which is consumed by an excessively draining blood clotting in the blood vascular system of coagulation factors and it eventually results in a tendency to bleed. DIC is a member of the vasculopathy.
Are used interchangeably, the terms coagulation and defibrination. These terms describe the pathogenesis of the clinical picture is incomplete.
Basics
→ Main article: hemostasis
If, due to injury of the blood vessels, bleeding, then to prevent the excessive leakage of blood, a complex system, the so-called " intrinsic system ", consisting of the blood platelets ( thrombocytes), the internal lining of the affected blood vessel ( vascular endothelium ), the tissue outside the vessel and clotting factors in the blood, plasma, activated. This is the basis for the healing of wounds. It is important that this process is limited to the site of injury and is not falsely triggered by other events such as inflammation or infection.
Due to the injury to the vessel wall underlying collagen is exposed. At this store to platelets, which consequently release substances that stimulate the one hand, more platelets to attach to the injury, and on the other hand, trigger the so-called coagulation cascade. As a result, formed a solid plug of fibrin, which closes the wound.
If pinging process unregulated and throughout the body, so it comes to consumption coagulopathy.
Causes and triggers
The DIC is not a disease, but occurs as an additional complication in a variety of different diseases. It is divided into an acute and a chronic form.
Causes the acute form are shock, severe sepsis, extensive burns and Polytraumatisierungen result of severe accidents. Furthermore, it can as a complication at birth, caused by septic abortion, placental abruption, amniotic fluid embolism, preeclampsia and eclampsia, occur. Other possible causes include blood poisoning ( caused by gram -negative bacteria, rickettsial diseases, viral diseases ), hemolytic syndromes, Organnekrosen (acute pancreatitis, acute hepatic necrosis ), and complications of surgery, particularly lung, pancreas, prostate, liver and heart.
The chronic form may occur as a complication of cirrhosis, in heart defects in metastatic carcinomas, with haematological malignancies ( especially acute leukemias ) and in congenital Riesenhämangiomen ( Kasabach -Merritt syndrome).
Stages of DIC
Stage 1: Pathological activation
Here, the non-physiological reaction is clinically and diagnostically nor compensated, that is, you can still see no deviation from the norm, even though the failure process has already been set in motion. TFPI (Tissue Factor Pathway Inhibitor ) and antithrombin, however, already consumed.
The coagulation is initiated by the pro-coagulant effect of various components of the coagulation cascade, which are released by abnormally high levels of endogenous mediators such as histamine, serotonin and adrenaline, by bacterial endotoxins or directly by the destruction of platelets in too large quantities.
In the field of blood capillaries, venules and arterioles occurs in the sequence for the formation of small blood clots ( microthrombi ), which block these blood vessels. Those most at risk are of this, the highly perfused organs lung, kidney and heart, and the function of the liver and adrenal glands can be affected.
Stage 2: Deficit
Now there is a significant decrease of platelets, coagulation factors and inhibitors - they are consumed. This is associated with fibrinolysis and laboratory- increased levels of fibrin and fibrin degradation products (D - dimer)
The undirected clotting within the vessels leads to a consumption of the necessary blood to clot blood components ( here especially lack of platelets ( thrombocytopenia), fibrinogen ( hypofibrinogenemia ), prothrombin and coagulation factors V, VIII and X). As a consequence of an organism is no longer able to seal damaged blood vessels independently. It comes to a bleeding tendency ( bleeding diathesis ).
Stage 3: defibrination
Platelets, coagulation factors and antithrombin are now greatly reduced. The result is the frame of a shock. This can be either with multi-organ failure associated ( by emboli / thrombi) or with a bleeding tendency, or with both, because now missing clotting factors to form thrombi, but also because the anti-clotting factors are consumed.
Fresh wounds no longer seal the deal. This leads to increased postoperative bleeding after surgery. Occur spontaneously bleeding, that is, Bleeding without serious accident, for example, in skin and mucous membranes, gastrointestinal tract, kidneys, and brain.
Therapy and prophylaxis
If the circulation of blood flow ( or other triggers ) → coagulation → Consumption of clotting material → → bleeding bleeding once in motion, it's hard to interrupt him. To prevent coagulation it would be theoretically necessary to prevent excessive clotting in patients at risk in accordance with heparin.
A positive effect of heparin has not been established for DIC in studies, it is therefore only for thrombosis prophylaxis, but not recommended for the therapy or prophylaxis of DIC. When bleeding (recombinant factor VIIa for example, factor XIII, AT III ) and severe thrombocytopenia and platelet concentrates, fresh frozen plasma can or individual factors are used. Heparin should not be used in case of a bleeding complication.
Most importantly, however, is the mastery of the underlying disorder ( eg, adequate treatment of sepsis, shock therapy).
Laboratory parameters
The most important laboratory parameters are thus D- dimer, platelet count and INR, and fibrinogen, which reach a value of ≥ 5 for a potentially manifest and <5 for a non- overt DIC based on a DIC score. However, these values must be considered in combination with the underlying disease.