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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.
ETIOLOGY
PATHOPHYSIOLOGY
Bleeding manifestations
o Petechiae, purpura, ecchymoses
o Oozing of blood from surgical wounds,intravenous lines
o Hematuria
o Hematemesis, hematochezia
o Collection of blood in body cavities: features of hemoperitoneum, hemothorax
Thrombotic manifestations
o Acute renal failure: oliguria
o Hepatic dysfunction: jaundice
o ARDS: dyspnea, rales
o Pulmonary thromboembolism: dyspnea, chest pain, hemoptysis
o Deep vein thrombosis: lower limb edema
o Neurological dysfunction: altered mental status, stroke
o Purpura fulminans: DIC with extensive skin necrosis
o Waterhouse Friderichsen syndrome: adrenal infarcts → adrenal insufficiency
Note: The clinical features of DIC may appear acutely (e.g., following trauma, sepsis), or may appear
subacutely (e.g., DIC following malignancy)!
DIAGNOSTICS
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!
↓ Hematocrit × × ✓ ×
Schistocytes × ✓ ✓ ×
(In the case of DIC, schistocytes
(fragmented erythrocytes) are seen in
association with microangiopathic
hemolytic anemia.)
DIFFERENTIAL DIAGNOSIS
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
Treatment of the underlying illness (e.g., antibiotics for infectious diseases, chemotherapy or
surgery for malignant disease)
Bleeding and consumptive types
o Transfusion of blood products
Platelet concentrate if:
Platelet count < 10,000 in asymptomatic individuals
Platelet count < 50,000 in patients with active bleeding or if a surgical procedure
is planned
Fresh frozen plasma if PT or APTT > 1.5 times the normal value
Cryoprecipitate if fibrinogen < 150 mg/dL
Packed RBCs if:
Massive hemorrhage without hemodynamic response to fluid therapy
Hb < 7 g/dL
If acute traumatic coagulopathy → transfuse packed RBC, FFP, and platelet
concentrate in a 1:1:1 ratio
o Synthetic protease inhibitor (e.g., Gabexate mesilate®, nafamostat®)
o Antifibrinolytic therapy (e.g., tranexemic acid)
Organ failure type: natural protease inhibitor (e.g., antithrombin, or rhTM administration)
Non-symptomatic type: heparin
Note: Treatment of the underlying disease forms the cornerstone of the management of DIC!