Disseminated intravascular coagulationD65.1
Synonym(s)
HistoryThis section has been translated automatically.
DefinitionThis section has been translated automatically.
Acquired breakdown of hemostasis involving platelets, epithelium, coagulation factors, fibrinolysis, inhibitors, complement and the kininogen system. The result is acute intravascular coagulation of varying aetiology with formation of numerous microthrombi, consumption of all coagulation active substances (platelets, fibrinogen, coagulation factors) and a consecutive tendency to bleed.
EtiopathogenesisThis section has been translated automatically.
Disseminated intravascular coagulation (DIC) is a disorder that can have many causes, all of which converge on a common etiopathogenetic final pathway. The basis of the disorder is a consumption of platelets, coagulants, and anticoagulants to an extent that can no longer be compensated by the synthesis of these substances . Therefore, localized or generalized hemorrhagic diatheses, thromboses in the microcirculation, tissue necrosis and multiple organ failures occur.
Triggers are often bacterial infections by streptococci, staphylococci, pneumococci, meningococci, gram-negative rods, but also viruses, parasites, rickettsiae or mycoses. Other causes are endothelial damage, e.g. in the context of a haemolytic-uraemic syndrome, acute glomerulonephritis or Rocky Mountain fever.
Other feared causes are obstetric complications such as placental abruption, amniotic fluid embolism, septic abortion, intrauterine amniotic death and eclampsia.
Other frequent causes are neoplasms such as adenocarcinomas, acute promyelocytic leukaemia, but also severe haemolyses. Furthermore, tissue damage, such as burns, frostbite and gunshot wounds, can trigger a consumption coagulopathy.
An important cause of DIC is acute promyelocytic leukemia. The leukemic promyelocytes produce a leukocyte elastase that proteolytically destroys alpha-2 antiplasmin, factor-V, fibrin, and plasmin. In addition, promyelocytes produce t-PA and urokinase.
Several fatal cases of disseminated intravascular coagulation have occurred during the current COVID-19 vaccination campaigns with Astra-Seneca 's vector vaccine . The fatal disseminated coagulation episodes occurred within a 14-day period after vaccination. Persons <55 years of age were affected more frequently. Women were affected more frequently ( EMA communication of 18.3.2021).
Clinical featuresThis section has been translated automatically.
LaboratoryThis section has been translated automatically.
TherapyThis section has been translated automatically.
Note(s)This section has been translated automatically.
A cause of DIC that is rare in Europe is the venom of the Malayan moccasin viper. It contains enzymes that destroy fibrin and have thrombin-like effects. These effects are not antagonizable by AT-III.
LiteratureThis section has been translated automatically.
- Chang JC (2018) Disseminated intravascular coagulation: is it fact or fancy?
Blood Coagul Fibrinolysis 29:330-337. - Dupuy M (1834) Injections de matière cérébrale dans les veines. Gaz Med Paris 2: 524
- Hengge UR et al (2002) Purpura fulminans. A fatal consequence of a widely used medication? dermatologist 53: 483-487
- Levi M et al (2003) Sepsis and disseminated intravascular coagulation. J Thromb thrombolysis 16: 43-47
- Lubach D, Barthels M (1984) Two-dimensional purpura with necroses in severe cases of consumption coagulopathy. Dermatologist 35: 152-158
- Rheingold SR et al (2004) HIV infection presenting as severe autoimmune hemolytic anemia with disseminated intravascular coagulation in an infant. J Pediatr Hematol Oncol 26: 9-12
- Slofstra SH et al (2003) Disseminated intravascular coagulation. Hematol J 4: 295-302
- Toh CH et al (2003) Disseminated intravascular coagulation: old disease, new hope. BMJ 327: 974-977
- Veiga AB et al (2003) Fibrinogenolytic and procoagulant activities in the hemorrhagic syndrome caused by Lonomia obliqua caterpillars. Thromb Res 111: 95-101