Disseminated Intravascular Coagulation
Also known as: DIC — Consumptive Coagulopathy
DIC, also known as consumptive coagulopathy, is a condition where the coagulation 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 as a secondary condition with an underlying cause. There are multiple aetiologies for DIC; once the cascade is under way the 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 reactions.
- Certain snake venoms.
- Acute haemolytic crises.
- Infections (viral, bacterial, protozoal) and post-infectious immunologic reactions.
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 rise; thrombin converts plasminogen into the active form, plasmin which initiates the fibrinolytic cascade. Fibrinolysis produces high levels of fibrin degradation products (FDPs) which are themselves anticoagulants, promoting further lysis. As thrombi form in the vasculature, tissues become hypoxic leading to multisystemic organ failure in severe cases.
As platelets are used up in the thrombi, a thrombocytopaenia occurs which leads to paradoxical haemorrhaging and the patient starts to shown symptoms of bleeding. This is the mechanism by which most viral haemorrahgic diseases induce clinical symptoms.
These are noted due to spontaneous primary bleeding, including 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.
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.
Can reveal an azotaemia and hyperphosphataemia, increased liver enzyme activity and if severe enough a hypoproteinaemia.
Will reveal a decreased PCV, a thrombocytopaenia and often a neutrophilia with a left shift.
Haemoglobinuria and bilirubinuria may be present. Do not undertake cystocentesis as this may lead to further bleeding.
Pro Thrombin (PT) and Partial Thromboplastin Time (PTT) increases. Fibrin degradation products (FDPs) are also increased and fibrinogen levels will decrease.
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.
DIC has a poor prognosis with a high mortality rate.
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