Disseminated Intravascular Coagulation

DIC, also known as consumptive coagulopathy, is a condition where the coaguation and fibrinolytic cascades are out of control. There is widespread clotting throughout the body with fibrinolysis and then a paradoxical haemorrhage.

There are multiple aetiologies for DIC, however, once the cascadeis under way the disease process is essentially the same. Causes include:

• Sepsis, particularly gram negative organisms.
• Obstetric complications; chemicals released from the uterus.
• Tissue trauma E.g. burns.
• Liver disease.
• Transfusion reaction.
• Neoplasia.
• Viral haemorrhagic fevers.
• Certain snake venoms.

Pathophysiology:

Once coagulation begins a positive feedback loop is set up whereby coagulation inhibitors are consumed, allowing more coagulation. In this way coagulation continues and induces further coagulation. Thrombin levels are increased. Thrombin converts plasminogen into the active form, plasmin and initiates the fibrinolytic cascade. Fibrinolysis produces high levels of FDPs (fibrin degradation products) which are themselves anticoagulants, further fuelling the coagulation cascade. As thrombi form in the vasculature tissues will become hypoxic leading to multisystemic organ failure in severe cases.

As platelets are used up in the thrombi a thrombocytopaenia occurs, leading to a paradoxical haemorrhage and the patient starts to bleed. This is the mechanism by which most viral haemorrahgic diseases cause their clinical signs.

DIC has a poor prognosis with a high mortality rate.

Treatment:

It is important to identify and treat the underlying cause of the DIC. Other treatments are limited;

• Anticoagulants should be used with caution as the patient will be prone to haemorrhage.
• Transfusion with fresh frozen plasma to provide clotting factors and platelets.

• Disseminated intravacular coagulation is a widespread intravascular coagulation of the microcirculation.
• The capillaries are principally affected.
• There are various causes.
  • Mismatched blood transfusion
  • Acute haemolytic crises
  • Extensive burns and trauma
  • Infectious and post-infectious immunologic reactions.
• There is widespread occlusion of the microcirculation with small white thrombi.
  • May cause shock, acute respiratory distress, heart failure or renal failure.
• Haemorrhagic diathesis may develop.
  • Is a result of rapid consumption and depletion of fibrinogen, platelets and clotting factors
• The fibrinolytic system is also highly stimulated to prevent what little clotting activity that remains.