Table 1.
Clinical condition | Pathogenetic trigger | |
---|---|---|
1 | Sepsis and severe infections – gram positive and negative bacteria, viruses, fungi, parasites | Exotoxins and endotoxins (lipopolysaccharides) |
2 | Crush injuries and sever trauma | Phospholipids and fats from damaged tissues; fat embolism |
3 | Head injury | Phospholipids and fats from damaged tissues |
4 | Acute severe pancreatitis | Cytokines and severe inflammatory response |
5 | Solid tumors – pancreatic and prostate carcinoma | Cancer procoagulant |
6 | Hematological malignancies | Tissue factor; cytokines |
7 | Transfusion related hemolytic reactions – ABO and Rh incompatibility | Widespread endothelial damage |
8 | Obstetrical complications – placental abruption, amniotic fluid embolism, eclampsia, HELLP syndrome, RPOC, septic abortion, fetal demise | Leakage of procoagulant substances from placenta and amniotic fluid; widespread endothelial damage |
9 | Vascular malformation – giant hemangiomas, aneurysms | Localized activation of platelet aggregation and coagulation; can become widespread |
10 | Snake bites | Hemorrhagic metalloproteinases; thrombin-like enzymes; factor X and prothrombin activators [53] |
11 | Heat stroke, hyperthermia, and burns | Tissue factor; protein alteration with temperature changes |
12 | Acute fulminant hepatic failure | Accelerated platelet and coagulation activation; decreased pro- and anticoagulant synthesis complicates DIC |
13 | Drugs – allergic reactions and overdoses such as amphetamines | Severe inflammatory or immunological response; tissue necrosis and rhabdomyolysis in case of amphetamines |
14 | Purpura fulminans | Acute DIC and hemorrhagic cutaneous necrosis |
Abbreviations: HELLP (hemolysis, elevated liver enzymes, and low platelets) RPOC (retained products of contraception), DIC (disseminated intravascular coagulation).