Disseminated Intravascular Coagulation

Also known as:

DIC

Description

DIC, also known as consumptive coagulopathy, is a condition where the coaguation and fibrinolytic cascades are out of control as a result of systemic thrombosis. There is widespread clotting throughout the body with fibrinolysis and then a paradoxical haemorrhage. It is often recognised in dogs but rarely in cats. DIC always occurs secondary to another disease. There are multiple aetiologies for DIC, however, once the cascade is 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.

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.

Clinical Signs

Present due to spontaneous primary bleeding and include Petechiae, ecchymoses, mucosal bleeding or secondary bleeding into body cavities e.g haemoabdomen. Ventricular arrythmias may also be present due to myocardial hypoxia or thrombosis.

Laboratory Tests

Blood Smear

Will see evidence of anaemia which can be regenerative or non-regenerative depending on the underlying cause of DIC. Also a neutrophilia with a left shift and thrombocytopaenia will be present. Schistocytes may also be seen due to haemolysis.

Biochemistry

Can reveal an azotaemia and hyperphosphataemia, increased liver enzyme activity and if severe enough a hypoproteinaemia.

Haematology

Will reveal a decreased PCV, a thrombocytopaenia and often a neutrophiia with a left shift.

Urinalysis

Haemoglobinuria and bilirubinuria may be present. Do not undertake cystocentesis as this may lead to further bleeding.

Clotting factors

Pro Thrombin (PT) and Partial Thromboplastin Time (PTT) increases. Fibrin degradation products (FDPs) are also increased and fibrinogen levels will decrease.

Treatment

It is important to identify and treat the underlying cause of the DIC. It is also important to ensure adequate tissue perfusion and support target organs susceptible to ischaemia and haemorrhage by fluid therapy. Anticoagulants should be used with caution as the patient will be prone to haemorrhage and blood components must be replaced via transfusion with fresh frozen plasma to provide clotting factors and platelets.

Prognosis

DIC has a poor prognosis with a high mortality rate.

• 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.