Disseminated intravascular coagulopathy
A disseminated intravascular coagulopathy (from Latin : disseminated “scattered”, intravascular “in the vessel ”, coagulation “coagulation”), DIC for short (as an abbreviation of the English term Disseminated Intravascular Coagulation ), also called disseminated intravascular coagulation ( DIG ), is a Acquired life-threatening condition, in which excessive blood clotting in the blood vessel system depletes coagulation factors and ultimately leads to a tendency to bleed . The DIC belongs to the group of vasculopathies .
The terms consumption coagulopathy and defibrination syndrome are used synonymously . These terms describe the pathogenesis of the clinical picture only incompletely.
→ Main article: hemostasis
If bleeding occurs due to an injury to blood vessels , a complex system consisting of the blood platelets , the inner lining of the affected blood vessel ( vascular endothelium ), the tissue outside the vessel as well as in the blood vessel is created in order to avoid the excessive leakage of blood Clotting factors contained in blood plasma are activated. This forms the basis for wound healing. It is important that this process is limited to the location of the injury and is not erroneously triggered by other events such as inflammation or infection.
The collagen underneath is exposed as a result of the damage to the vessel wall . Thrombocytes attach to this, which consequently release substances that, on the one hand, stimulate further thrombocytes to attach to the injury and, on the other hand, trigger the so-called coagulation cascade . As a result, a solid plug of fibrin is created that closes the wound.
If this process runs unregulated and throughout the body, consumption coagulopathy occurs.
Causes and Triggers
Consumption coagulopathy is not an independent disease, but occurs as an additional complication in a large number of different clinical pictures. A distinction is made between an acute and a chronic form.
The causes of the acute form are shock , severe sepsis , extensive burns and multiple traumas as a result of severe accidents. It can also occur as a complication in childbirth , triggered by septic abortion , premature placental abruption, amniotic fluid embolism , preeclampsia and eclampsia . Other possible causes are blood poisoning (due to gram-negative germs, rickettsioses , viral diseases), hemolytic syndromes , organ necrosis ( acute pancreatitis , acute liver necrosis ) and complications of surgical interventions, especially on the lungs , pancreas , prostate , liver and heart .
The chronic form can occur as a complication of liver cirrhosis , heart defects , metastatic carcinomas , hemoblastoses (especially acute leukemia ) and congenital giant hemangiomas ( Kasabach-Merritt syndrome ).
Stages of DIC
- Pathological activation of the coagulation system
- Noticeable deficit in the coagulation potential
1st stage: pathological activation
Here, the non-physiological reaction is clinically and diagnostically compensated, that is, no deviation from the norm can be recognized, although the wrong process has already been started. However, tissue factor pathway inhibitor (TFPI) and antithrombin are already being used up.
Consumption coagulopathy is initiated by the coagulation-promoting effect of various components of the coagulation cascade , which are released in excessive amounts by an abnormally high level of the body's own messenger substances such as histamine , serotonin and adrenaline , by bacterial endotoxins or directly by the destruction of blood platelets .
As a result, small blood clots ( microthrombi ) form in the area of blood capillaries , venules and arterioles , which block these blood vessels. The organs with high blood flow are the lungs , kidneys and heart , and the function of the liver and adrenal glands can also be severely impaired. The cardiac output decreases.
2nd stage: deficit
Now there is a significant drop in platelets, coagulation factors and inhibitors - they are used up. This goes hand in hand with fibrinolysis and laboratory diagnostic elevated values for fibrin breakdown products ( D-dimer ) and a decrease in fibrin .
The non-directional coagulation within the vessels leads to the consumption of blood components necessary for blood coagulation, in particular a lack of platelets ( thrombocytopenia ), fibrinogen (hypofibrinogenemia), prothrombin complexes and the coagulation factors V, VIII and X. As a consequence, the organism is no longer able to close damaged blood vessels on their own. There is a tendency to bleed ( hemorrhagic diathesis ).
3rd stage: defibrination
Platelets , clotting factors and antithrombin are now greatly reduced. The result is a full picture of a shock. This can be associated either with multiple organ failure (due to embolism / thrombi) or with a tendency to bleed or with both, since the coagulation factors are now missing to form thrombi, but also because the anticoagulant factors have been used up.
Fresh wounds no longer close. There is increased bleeding after surgery. Bleeding occurs spontaneously, ie bleeding without corresponding injury, for example in the skin and mucous membranes, stomach, intestines, kidneys and brain.
Therapy and prophylaxis
Once the bleeding cycle (or other trigger) → blood coagulation → consumption of coagulation material → bleeding tendency → bleeding is in motion, it is difficult to interrupt it. In order to prevent consumption coagulopathy, it would theoretically be necessary to avoid excessive coagulation with heparin in patients who are at risk .
However, studies have not demonstrated a positive effect due to heparin for DIC, so it is only recommended for thrombosis prophylaxis, but not for therapy or prophylaxis of DIC. In the case of bleeding, thawed frozen fresh plasma or individual factors (e.g. factor XIII, AT III, recombinant factor VIIa) and in severe thrombocytopenia also platelet concentrates can be used. Heparin should no longer be used in the event of a bleeding complication.
Most important, however, is mastery of the underlying disorder (e.g. adequate therapy for sepsis, shock therapy).
The most important laboratory parameters are accordingly D-dimer , platelet count and Quick value as well as fibrinogen , which on the basis of a DIC score achieve a value of ≥ 5 for a possibly manifest and <5 for a non-manifest DIC. However, these values must be viewed in combination with the underlying disease.
|Platelet count||> 100,000 / µl||0|
|50,000 - 100,000 / µl||1|
|<50,000 / µl||2|
|Fibrinogen levels||more than 100 mg / dl||0|
|less than 100 mg / dl||1|
- Dimitrios A. Tsakiris: Causes and pathogenesis of disseminated intravascular coagulation (DIC) . Switzerland Med Forum 2004; 4: 1109–1112. Online version (PDF; 216 kB).
- C.-E. Dempfle, M. Borggrefe: Disseminated intravascular coagulation . Intensivmed 43: 103-110 (2006)
- Laborlexikon: Quick value >> Specialist knowledge for everyone! << . Retrieved April 28, 2014.
- ISTH SSC reference tools . Retrieved August 24, 2018.
- Adam Brochert: Pathology I case by case . Elsevier, Urban & Fischer Verlag 2005, p. 46ff.
- Hans Peter Schuster: Diagnostics and intensive therapy for sepsis and multiple organ failure . Springer Verlag 2006, pp. 70ff.
- Harald Renz: Practical laboratory diagnostics: textbook on laboratory medicine, clinical chemistry and hematology. Berlin [u. a.]: de Gruyter; 2009 p. 150ff.