Disseminated intravascular coagulation

Last updated: August 17, 2023

Summarytoggle arrow icon

Disseminated intravascular coagulation (DIC) is a disorder characterized by systemic activation of the extrinsic clotting cascade with microthrombi formation, platelet consumption, and subsequent exhaustion of all clotting factors. Common causes of DIC include sepsis, trauma, and malignancy. Depending on the underlying pathophysiological processes and subtype, patients present with signs of bleeding (e.g., purpura, petechiae, ecchymoses) and/or multiorgan failure. Laboratory studies can be highly variable. However, typical findings in overt decompensated DIC include thrombocytopenia, prolonged PT and aPTT, decreased fibrinogen levels, and elevated D-dimer levels. Treatment involves identification of the underlying cause and supportive therapy with transfusions of blood products (pRBCs, platelet concentrates, FFP, and/or cryoprecipitate) and, in select cases, anticoagulants (e.g., heparin) or antifibrinolytic therapy (tranexamic acid). Close monitoring and specialist consultation (e.g., critical care and hematology) are typically required.

Overviewtoggle arrow icon

Disseminated intravascular coagulation (DIC)

  • Definition: a syndrome characterized by thrombosis, hemorrhage, and organ dysfunction caused by systemic activation of the clotting cascade, which leads to platelet consumption and exhaustion of clotting factors
  • Latent DIC: no overt symptoms (little to no bleeding, increased risk of thrombotic events, laboratory abnormalities)
  • Overt DIC: clear signs and symptoms (e.g., bleeding, thrombosis) that depend on the balance of the deranged processes

According to disease onset [1]

Consumption coagulopathy

Etiologytoggle arrow icon

The mnemonic “STOP Making Trouble!” helps to recall the etiology of DIC: SSepsis/Snakebites, TTrauma (acute traumatic coagulopathy), OObstetric complications, PPancreatitis, MMalignancy, TTransfusion.


Classificationtoggle arrow icon

The 2014 International Society of Thrombosis and Haemostasis (ISTH) harmonized guidelines distinguish between DIC types based on clinical phenotype, characteristic laboratory abnormalities, and treatment targets.

Overview of DIC types [3][4][5][6]


Suggestive laboratory findings Potential therapeutic targets
Nonsymptomatic type DIC
  • Symptoms: little to none
  • Predominant mechanism: low-grade fibrinolysis and/or hypercoagulation
  • Typical underlying diseases: variable
Bleeding type DIC
Massive bleeding type DIC
Organ failure type DIC

TAT: Thrombin antithrombin complex, PPIC: Plasmin α2-plasmin inhibitor complex, PAI-1: Plasminogen activator inhibitor-1, PT: Prothrombin time, FDPs: Fibrin degradation products, FFP: Fresh frozen plasma, pRBC: Packed red blood cells

Pathophysiologytoggle arrow icon

Overview [3][4][5]


Clinical featurestoggle arrow icon

Clinical features are variable and depend on the predominant underlying mechanism. [7]

The clinical features of DIC may appear acutely (e.g., following trauma, sepsis) or subacutely (e.g., DIC following malignancy).

Diagnosticstoggle arrow icon

General principles [6][8]

  • Suspect DIC based on clinical features and typical underlying diseases; especially in patients with clinical deterioration.
  • Laboratory studies vary depending on the subtype, underlying disorders, and stage of DIC.
  • Challenges
    • No single test can reliably rule out DIC.
    • Nonsymptomatic DIC may only become apparent after specific laboratory screening.
    • DIC may already be irreversibly decompensated by the time diagnosis is made using scoring systems.
    • Many conditions can manifest with similar laboratory abnormalities (see “Differential diagnoses of DIC by laboratory findings”).

Laboratory studies [5][6][9]

Routine laboratory tests

The diagnosis of DIC is not based on a single marker but on a combination of laboratory findings. Thrombocytopenia, elevated D-dimer, increased PT and aPTT, and low fibrinogen should immediately raise suspicion for DIC. [9]

Specialized tests [5]

The following tests should be considered on a case-by-case basis in consultation with a specialist (e.g., intensivist, hematologist).

International Society of Thrombosis and Haemostasis (ISTH) DIC score [5][9][11]

  • Multiple scoring systems exist, each with advantages and disadvantages that depend on the underlying cause of DIC. [2]
  • The ISTH DIC score identifies patients with a high likelihood of overt DIC. It can only be used in patients with a known predisposing disease.

ISTH DIC score [12]

Criteria Level Points assigned
Platelet count > 100,000/mm3 0
50,000–100,000/mm3 1
< 50,000/mm3 2
Increase in fibrin markers (D-dimer, soluble fibrin, other FDPs) None 0
Moderate 2
Strong 3
Prothrombin time prolongation < 3 seconds 0
3–6 seconds 1
> 6 seconds 2
Fibrinogen ≥ 100 mg/dL 0
< 100 mg/dL 1


Differential diagnosestoggle arrow icon

Differential diagnoses by laboratory findings [1]

Differential diagnoses of DIC by laboratory findings [1][6][13]

Condition Platelets Bleeding time PT aPTT Fibrinogen D-dimer/FDPs
DIC Typically low but can be variable [14]
Thrombotic microangiopathy (TTP, HUS, HELLP syndrome)





Normal or ↑

Normal or ↑

Normal or ↑






Normal or ↑
Liver disease

Normal or ↓

Normal or ↑

Normal or ↓

Normal or ↑
Vitamin K deficiency or warfarin use



Normal or ↑



Differential diagnoses by underlying process

The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon

General principles [5][9]

  • First-line: treatment of the underlying disease (see “Etiology”)
  • Additional treatment depends on the subtype and is complicated (see “Overview of DIC types”). Involve specialists early.
  • Supportive therapy
    • Avoid invasive procedures if possible
    • Vitamin K supplementation if deficiency is suspected [3]
  • Initiate clinical and serial laboratory monitoring to assess response to treatment.

Treatment recommendations by type of DIC [3][5]

Type Generally recommended Generally discouraged
Nonsymptomatic type DIC
Organ failure type DIC
  • Anticoagulation: Consider therapeutic heparin.
  • Consider advanced treatments.
Bleeding type DIC
Massive bleeding type DIC

Treatment of the underlying disease is the cornerstone of management.

Blood products [5][6][9][9][16]

The decision to transfuse blood products should primarily be based on the presence or risk of bleeding. Laboratory parameters can be used as a treatment goal but should not be considered the sole rationale for transfusion. Involve specialists early.

Antifibrinolytic therapy [5][16]

Aminocaproic acid is generally contraindicated in DIC.

Anticoagulation [5][9][11][16][20]

Patients receiving anticoagulants require careful monitoring of bleeding events and dosage adjustment for BMI and kidney function.

Warfarin is ineffective and possibly harmful in DIC, as it inhibits production of protein C and protein S, which can worsen coagulopathy. [22][23]

Fibrinolytic therapy (e.g., tPA) should be avoided in all types of DIC. [3][5]

Acute management checklisttoggle arrow icon

All patients [5][16]

  • Consider DIC in patients with an associated underlying condition and clinical deterioration.
  • Order CBC and serial coagulation tests (including PT, aPTT, fibrinogen, D-dimer and other FDPs).
  • Consider calculating the ISTH DIC score to support the diagnosis.
  • Rule out differential diagnoses.
  • Consult hematology and intensive care as needed.
  • Consider ordering specialized tests according to DIC type.
  • Identify and treat the underlying cause.
  • Monitor coagulation parameters frequently.
  • Avoid invasive procedures if possible.
  • Supplement vitamin K if there is a suspected deficiency.

Bleeding type DIC or massive bleeding type DIC

Nonsymptomatic type DIC and organ failure type DIC

Referencestoggle arrow icon

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  2. Asakura H. Classifying types of disseminated intravascular coagulation: clinical and animal models. J Intensive Care. 2014; 2 (1): p.20.doi: 10.1186/2052-0492-2-20 . | Open in Read by QxMD
  3. Papageorgiou C, et al. Disseminated Intravascular Coagulation: An Update on Pathogenesis, Diagnosis, and Therapeutic Strategies. Clinical and Applied Thrombosis/Hemostasis. 2018; 24 (9_suppl): p.8S-28S.doi: 10.1177/1076029618806424 . | Open in Read by QxMD
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  6. Levi M, et al. Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology.. Br J Haematol. 2009; 145 (1): p.24-33.doi: 10.1111/j.1365-2141.2009.07600.x . | Open in Read by QxMD
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