**7.1. Disseminated intravascular coagulation (DIC)**

DIC is characterized by activation of clotting system within the vasculature which blocks the micro vessels and can cause further organ dysfunction [125]. In contrast, it can also accelerate fibrinolysis and cause severe bleeding. The international Society of Hematology (ISTH) has defined DIC as *"an acquired syndrome characterized by the intravascular activation of coagulation with loss of localization arising from different causes. It can originate from and cause damage to microvasculature, which if severe, can produce organ dysfunction"* [125–127]. DIC occurs in all ages, races and all genders. DIC is classified as acute DIC, developed due to sudden exposure of procoagulants [125–127]. In acute DIC compensatory hemostatic mechanisms are quickly overwhelmed and leads to hemorrhage development. Chronic DIC is develops due to constant or intermittent exposure of small amounts of tissue factor (TF) [125–127]. DIC is acquired due to several reasons which include external agents such as infections, snake bite, trauma, severe transfusion reactions and environmental changes that cause hemocytopenia [125–127]. Disease conditions leading to DIC include malignancy, organ disfunctions such as hepatic failure and pancreatitis, vascular abnormalities. The phenotypes of DIC include non-symptomatic, bleeding, massive bleeding and organ failure type. If there is no observed phenotype in the patients, whereas the abnormalities were observed in clinical laboratory only, the diagnosis is known as Non-symptomatic DIC [125–127]. In the bleeding type is more predominantly observed phenotype in DIC, the primary symptom is bleeding due to hyperfibrinolysis [125–127]. This phenotype is observed in patients with leukemia, aortic aneurysm and obstetric diseases. Organ failure phenotype is observed in the patients with hypercoagulation, this phenotype is observed in patients with infections. Massive bleeding is observed when the fibrinolysis and hypercoagulation are remarkable. Massive bleeding often leads to death [125–127].

DIC is diagnosed by global tests such as platelet count, prothrombin time (PT), aPTT and the amount of fibrinogen, fibrin and fibrin degradation products. Other diagnostic markers include antithrombin, Protein C, Thrombin-Antithrombin (TAT) complex, VWF propeptide and plasminogen activator inhibitor-1 (PAI-1) (**Table 2**). Treatment of DIC depends on the type of phenotype (**Table 2**) [128]. Heparin treatment is recommended for the treatment of non-symptomatic type whereas, antifibrinolytic treatment is not recommended. The recommended treatment for the organ failure type DIC is natural protease inhibitor whereas, antifibrinolytic treatment is not recommended [128]. Recommended treatments for the bleeding phenotype DIC include blood transfusion, synthetic protease inhibitors and a fibrinolytic treatment, the non-recommended treatments include heparin and anti-Xa [128] (**Figure 3**).
