Difference between revisions of "Disseminated Intravascular Coagulation"
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*Tissue trauma e.g. burns. | *Tissue trauma e.g. burns. | ||
*Liver disease. | *Liver disease. | ||
− | *[[Blood_Collection_for_Transfusion#Adverse_Reactions|Transfusion]] | + | *[[Blood_Collection_for_Transfusion#Adverse_Reactions|Transfusion reactions]]. |
*Neoplasia. | *Neoplasia. | ||
*Certain snake venoms. | *Certain snake venoms. |
Revision as of 08:42, 30 September 2010
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Also known as: DIC or Consumptive coagulopathy
Introduction
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 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.
- Neoplasia.
- 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 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.
Diagnosis
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 neutrophilia 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.
Literature Search
Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).
Disseminated Intravascular Coagulation publications