- Clinical science
Disseminated intravascular coagulation (DIC) is a disorder characterized by systemic activation of the clotting cascade with microthrombi formation, platelet consumption, and subsequent exhaustion of all clotting factors, which causes hemorrhagic manifestations. The most common causes are sepsis, trauma, and malignancy. Patients present with bleeding manifestations (e.g., purpura), and/or signs of multiorgan failure. Laboratory studies show thrombocytopenia, prolonged PT and aPTT, decreased fibrinogen levels, and increased D-dimer. Treatment of DIC involves treatment of the underlying cause, and supportive therapy with transfusions of platelet concentrates, FFP, and/or cryoprecipitate.
- (more commonly with gram-negative organisms)
- Acute traumatic coagulopathy
- Acute hemolytic transfusion reaction (AHTR)
- Traumatic brain injury
- Obstetric complications
- Heat stroke
- Intravascular hemolysis (e.g., acute transfusion reaction)
- Extracorporeal procedures (e.g.,, dialysis)
- Toxins: snake bites, amphetamine overdose
- Vascular malformations: aortic aneurysms
|Types of DIC||Bleeding (hyperfibrinolytic) type||Organ-failure (thrombotic) type||Massive bleeding (consumptive) type||Non-symptomatic DIC|
|Common causes|| |
|Clinical manifestation|| || || || |
DIC is an acquired coagulopathy that is frequently seen in hospitalized individuals!
- Bleeding manifestations
- ARDS: dyspnea, rales
- Pulmonary thromboembolism: dyspnea, chest pain, hemoptysis
- Deep vein thrombosis: lower limb edema
- Neurological dysfunction: altered mental status, stroke
- Purpura fulminans: DIC with extensive skin necrosis
- Waterhouse Friderichsen syndrome: adrenal infarcts → adrenal insufficiency
The clinical features of DIC may appear acutely (e.g., following trauma, sepsis), or may appear subacutely (e.g., DIC following malignancy)!
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!
|Finding||Type of DIC|
|Bleeding type||Organ failure type||Consumptive type||Non-symptomatic type|
|Thrombocytopenia → ↑ bleeding time||✓||✓||✓||✓|
|↑ Markers of fibrin breakdown (D-dimer, or FDP)|| |
|↑ PT and APTT|| |
|↓ Fibrinogen levels||✓||×||✓||×|
|↓ Antithrombin|| |
- Severe hepatic dysfunction: clinical features, and/or laboratory findings of liver injury, normal factor VIII assay
- Thrombotic thrombocytopenic purpura/immune thrombocytopenic purpura: no consumption coagulopathy → normal PT, aPTT
- Heparin-induced thrombocytopenia: history of heparin use, heparin-PF4 (HIT) antibodies in serum
All coagulation factors would be decreased in patients with DIC!
The differential diagnoses listed here are not exhaustive.
- Treatment of the underlying illness (e.g., antibiotics for infectious diseases, chemotherapy or surgery for malignant disease)
Bleeding and consumptive types
Transfusion of blood products
- Platelet concentrate if:
- Fresh frozen plasma if PT or APTT > 1.5 times the normal value
- Cryoprecipitate if fibrinogen < 150 mg/dL
- Packed RBCs if:
- If acute traumatic coagulopathy → transfuse packed RBC, FFP, and platelet concentrate in a 1:1:1 ratio
- Synthetic protease inhibitor (e.g., Gabexate mesilate®, nafamostat®)
- Antifibrinolytic therapy (e.g., tranexemic acid)
- Transfusion of blood products
- Organ failure type: natural protease inhibitor (e.g., antithrombin, or rhTM administration)
- Non-symptomatic type: heparin
Treatment of the underlying disease forms the cornerstone of the management of DIC!