Disseminated Intravascular Coagulation (DIC)

How to Cite This Chapter: Crowther M, Windyga J. Disseminated Intravascular Coagulation (DIC). McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. https://empendium.com/mcmtextbook/chapter/B31.II.15.21. Accessed July 18, 2024.
Last Updated: May 17, 2019
Last Reviewed: May 17, 2019
Chapter Information

Definition, Etiology, PathogenesisTop

Disseminated intravascular coagulation (DIC) is a syndrome that may develop in the course of various clinical conditions. DIC is a result of generalized activation of coagulation with a concomitant activation or inhibition of fibrinolysis.

1. Causes:

1) Acute DIC: Sepsis, severe infection (particularly in patients with hyposplenism), trauma (particularly extensive, multiorgan trauma or trauma causing fat embolism), internal organ injury (eg, acute pancreatitis, acute liver failure), obstetric complications (premature placental abruption, amniotic fluid embolism, preeclampsia), posttransfusion reactions, transplant rejection, snake bites, and sometimes cancer (acute promyelocytic leukemia [APL]).

2) Chronic DIC: Cancer (solid tumors), giant hemangiomas (Kasabach-Merritt syndrome), and large aortic aneurysms.

2. Pathogenesis: The generalized activation of coagulation may develop due to the following:

1) General effects of proinflammatory cytokines, for instance, in sepsis or major trauma, which lead to impairment of the anticoagulant effects of protein C, activation of platelets, and inhibition of fibrinolysis.

2) Circulating procoagulants, for instance, in the case of obstetric complications or cancer (in patients with APL or prostate cancer, activation of coagulation may be offset by a very severe activation of fibrinolysis).

3. Consequences:

1) Multiple thrombi in the microcirculation and (less frequently) in major vessels, which cause ischemic multiorgan injury.

2) Consumption of platelets, fibrinogen, and other coagulation factors, which leads to their deficiency and bleeding.

Clinical Features and Natural HistoryTop

Acute DIC has a rapid clinical course associated with severe bleeding (from surgical wounds, nasal and oral mucosa, genitourinary tract, and sites of vascular access), ischemic organ injury (renal failure, liver failure, respiratory insufficiency), and in some cases with shock and stroke (either hemorrhagic or ischemic).

Chronic DIC is associated with a spectrum of bleeding complications and may be clinically innocuous.


Diagnosis is based on serial measurements of parameters of hemostasis in a patient with a condition that may cause DIC. There is no single diagnostic laboratory test. Diagnosis of the cause of DIC (underlying condition) is essential.

1. Acute DIC: Unexplained thrombocytopenia (generally 50×109/L to 100×109/L); prolonged prothrombin time (PT)/international normalized ratio (INR), activated partial thromboplastin time (aPTT), and thrombin time; low serum levels of fibrinogen (in patients with sepsis this feature may be absent or develop late, because fibrinogen is an acute-phase protein and its levels may be transiently normal or elevated) and other coagulation factors; elevated D-dimer levels.

2. Chronic DIC: Usually suspected due to a mild to moderate platelet count reduction. Other laboratory measures are similar to acute DIC, although findings may be less marked.

Differential Diagnosis

Immune thrombocytopenia (including heparin-induced thrombocytopenia), thrombotic thrombocytopenic purpura, and hemolytic-uremic syndrome (these are differentiated by severe thrombocytopenia with normal coagulation profiles), primary or secondary hyperfibrinogenolysis, catastrophic antiphospholipid syndrome. Purpura fulminans mimics DIC but has very different treatment requirements.


1. Treatment of the underlying condition (eg, sepsis).

2.  Transfusions of blood products when indicated:

1) In patients with significant blood loss, transfuse packed red blood cells.

2) In patients with active bleeding (or those requiring an invasive procedure) and a prolonged aPTT or PT/INR (>1.5 × normal), administer fresh-frozen plasma.

3) In patients with a plasma fibrinogen level <1 g/L and bleeding, administer cryoprecipitate or fibrinogen concentrate; administration can be titrated against the fibrinogen level.

4) In patients with platelet counts <50×109/L and severe bleeding, administer platelet concentrate. Prophylactic transfusion is not indicated except in cases of very severe thrombocytopenia (<10×109/L), as the transfused platelets will be rapidly consumed and repeated exposure to donor platelets will cause refractoriness to subsequent transfusion. Poor response to platelets should be expected.

3. Drugs that may be considered:

1) The role of heparin (or low-molecular-weight heparin [LMWH]) in the treatment of DIC is controversial. Heparin is indicated in chronic, compensated DIC with predominant thrombosis. It may be effective in pregnant patients with fetal death syndrome and hypofibrinogenemia before induction of delivery or in patients with severe hemorrhage from a giant hemangioma or aortic aneurysm before planned resection. Consider using therapeutic doses of heparin in patients with DIC with predominant arterial or venous thrombosis or with severe fulminant purpura with symptomatic occlusion of cutaneous vessels. Unfractionated heparin (UFH) is administered IV (without an initial bolus) at a dose of 500 IU/h (or 10 IU/kg/h). Subcutaneous injections of prophylactic doses of UFH or LMWH reduce the severity of bleeding in patients with chronic DIC and are indicated in the prevention of venous thromboembolism in severely ill patients with acute DIC without active bleeding.

2) Tranexamic acid (a fibrinolysis inhibitor) 10 to 15 mg/kg IV is indicated only in very rare cases of DIC with severe fibrinolysis (in patients with APL, prostate cancer, and in some patients with Kasabach-Merritt syndrome). Absolute contraindications include hematuria, renal failure, features of ischemic organ injury, and chronic DIC.

A variety of experimental treatments are used in patients with DIC, such as antithrombin concentrates; however, evidence to support their use is limited. These treatment options should be confined to expert centers in patients with measured deficiency of these factors.

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