Medicine & USMLE

Disseminated Intravascular Coagulation (In Progress)

Platelet Disorders
  1. Platelet Plug Formation
  2. Bernard-Soulier Syndrome
  3. Glanzmann Thrombasthenia
  4. Immune Thrombocytopenic Purpura (ITP)
  5. Thrombotic Thrombocytopenic Purpura (TTP)
  6. Hemolytic Uremic Syndrome (HUS)
  7. Disseminated Intravascular Coagulation (In Progress)
  8. Von Willebrand Disease (In Progress)


Disseminated Intravascular Coagulation, or DIC for short, is a condition in which blood clots form throughout the body, blocking small blood vessels. DIC has many causes, including snake bites, sepsis, trauma, or even cancer. Regardless of the cause, DIC causes widespread release of procoagulant factors throughout the bloodstream, resulting in the formation of many abnormal blood clots all throughout the body. These abnormal blood clots consume large amounts of platelets and clotting factors, which leave less available in the circulation to actually function in stopping bleeding.

The classic clinical picture in patients is severe bleeding from all orifices - especially at IV sites, the nose, mouth, and anus. Excessive consumption of platelets and clotting factors causes a decreased circulating platelet count, as well as decreased circulating levels of Factors VIII, V, and I -- also known as fibrinogen. An increased bleeding time is also seen, reflecting a decrease in functional platelets. PT and PTT are both increased, reflecting impairments in the coagulation cascade. Blood clot formation in small vessels can shear red blood cells, resulting in hemolysis and the appearance of schistocytes on peripheral blood smears. Finally, D-dimer levels are increased, reflecting an overall increase in blood clot formation and breakdown in the body.

Key Points

  • Disseminated Intravascular Coagulation (DIC)
    • Pathogenesis
      • Release of procoagulants → widespread abnormal clotting → consumption of platelets and clotting factors → susceptibility to bleeding
      • Microthrombi formation can also cause mechanical shearing of RBCs → microangiopathic hemolysis
      • Causes
        • Snake bites
        • Sepsis (gram negative)
        • Trauma
        • Obstetric complications
        • Acute pancreatitis
        • Malignancy (e.g. AML)
        • Nephrotic Syndrome
        • Transfusion
    • Presentation
      • Bleeding from all orifices
        • E.g. catheter sites and mucosal surfaces
      • Purpura fulminans, petechiae and ecchymoses
        • Purpura fulminans is coagulation of blood vessels under the skin with subsequent skin necrosis
      • Multi-organ failure
        • Altered mental status
        • Dyspnea and shortness of breath
        • Renal and hepatic failure
      • Shock
        • Hypotension, tachycardia
    • Diagnosis
      • Decreased platelet count
        • Due to consumption of platelets in microthrombi
      • Increased bleeding time
        • Decreased platelet count increases laboratory measure of time to platelet plug (primary hemostasis)
      • Increased PT and PTT
        • Consumptive use of clotting factors causes increased laboratory measurement of all coagulation times
      • Schistocytes (helmet cells)
        • Seen on peripheral blood smear
      • Increased D-dimer
        • Degradation (split) product of fibrin, due to increased breakdown of cross-linked fibrin
      • Decreased fibrinogen levels
        • Due to consumption of all clotting factors
      • Decreased factors V and VIII
        • Due to consumption of all clotting factors
    • Treatment
      • Treat underlying disorder
      • Supportive
        • Fluids
        • Blood products (PRBCs, platelets, FFP)