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. 2017 Jul 13;7(3):157–167. doi: 10.1080/20009666.2017.1335156

Table 1.

Various clinical conditions associated with DIC and their pathogenesis.

  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).