Difference between revisions of "Disseminated Intravascular Coagulation"
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− | + | Also known as: '''''DIC — Consumptive Coagulopathy''''' | |
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− | == | + | ==Introduction== |
− | + | 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|thrombosis]]. There is widespread clotting throughout the body with fibrinolysis and then a paradoxical [[Haemorrhage|haemorrhage]]. It is often recognised in dogs but rarely in cats. | |
− | DIC, also known as | + | DIC always occurs as a secondary condition with an underlying cause. |
− | DIC always occurs secondary | + | There are multiple aetiologies for DIC; once the cascade is under way the process is essentially the same. Causes include: |
− | There are multiple aetiologies for DIC | ||
*Sepsis, particularly gram negative organisms. | *Sepsis, particularly gram negative organisms. | ||
*Obstetric complications; chemicals released from the uterus. | *Obstetric complications; chemicals released from the uterus. | ||
− | *Tissue trauma | + | *Tissue trauma e.g. burns. |
*Liver disease. | *Liver disease. | ||
− | *Transfusion | + | *[[Administering_a_Blood_Transfusion#Adverse_Reactions|Transfusion reactions]]. |
*Neoplasia. | *Neoplasia. | ||
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*Certain snake venoms. | *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. | + | Once [[Normal_Mechanisms_of_Haemostatic_Control#Coagulation_physiology|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 | + | 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 thrombi form in the vasculature tissues | ||
− | As platelets are used up in the thrombi a thrombocytopaenia occurs | + | As [[Thrombocytes|platelets]] are used up in the thrombi, a [[Platelet Abnormalities#Thrombocytopaenia|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. |
− | + | ==Clinical Symptoms== | |
− | + | These are noted due to spontaneous primary bleeding, including petechiae, ecchymoses, mucosal bleeding or secondary bleeding into body cavities e.g. [[Haemoabdomen|haemoabdomen]]. | |
− | ==Clinical | + | [[:Category:Altered Ventricular Impulse Formations|Ventricular arrythmias]] may also be present due to myocardial hypoxia or thrombosis. |
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− | Ventricular arrythmias may also be present due to myocardial hypoxia or thrombosis. | ||
==Laboratory Tests== | ==Laboratory Tests== | ||
===Blood Smear=== | ===Blood Smear=== | ||
− | Will see evidence of anaemia which can be regenerative or non-regenerative depending on the underlying cause of DIC. | + | Will see evidence of [[Regenerative and Non-Regenerative Anaemias|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. | + | Also a [[Neutrophilia|neutrophilia]] with a left shift and thrombocytopaenia will be present. Schistocytes may also be seen due to haemolysis. |
===Biochemistry=== | ===Biochemistry=== | ||
− | Can reveal an azotaemia and hyperphosphataemia, increased liver enzyme activity and if severe enough a hypoproteinaemia. | + | Can reveal an [[Azotaemia|azotaemia]] and hyperphosphataemia, increased [[Liver - Anatomy & Physiology|liver]] enzyme activity and if severe enough a hypoproteinaemia. |
===Haematology=== | ===Haematology=== | ||
− | Will reveal a decreased PCV, a thrombocytopaenia and often a | + | Will reveal a decreased PCV, a thrombocytopaenia and often a neutrophilia with a left shift. |
===Urinalysis=== | ===Urinalysis=== | ||
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===Clotting factors=== | ===Clotting factors=== | ||
− | Pro Thrombin and Partial Thromboplastin Time | + | Pro Thrombin (PT) and Partial Thromboplastin Time (PTT) increases. |
Fibrin degradation products (FDPs) are also increased and fibrinogen levels will decrease. | Fibrin degradation products (FDPs) are also increased and fibrinogen levels will decrease. | ||
==Treatment== | ==Treatment== | ||
− | + | It is important to identify and treat the underlying cause of the DIC. | |
− | 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 | + | It is also important to ensure adequate tissue perfusion and support target organs susceptible to [[Ischaemia|ischaemia]] and haemorrhage by [[Principles of Fluid Therapy|fluid therapy]]. |
− | Anticoagulants should be used with caution as the patient will be prone to haemorrhage and blood | + | Anticoagulants should be used with caution as the patient will be prone to haemorrhage and blood components must be replaced via [[:Category:Transfusion Medicine|transfusion]] with fresh frozen [[Plasma|plasma]] to provide clotting factors and platelets. |
==Prognosis== | ==Prognosis== | ||
DIC has a poor prognosis with a high mortality rate. | DIC has a poor prognosis with a high mortality rate. | ||
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+ | {{Learning | ||
+ | |literature search = [http://www.cabdirect.org/search.html?q=title%3A%28%22Disseminated+Intravascular+Coagulation%22%29+OR+title%3A%28%22Consumptive+coagulopathy%22%29+OR+title%3A%28DIC%29+OR+title%3A%28%22Disseminated+intravascular+coagulopathy%22%29 Disseminated Intravascular Coagulation publications] | ||
+ | }} | ||
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+ | {{review}} | ||
+ | {{OpenPages}} | ||
[[Category:Cardiovascular_System_-_Vascular_Pathology]][[Category:Cardiovascular_System_-_Inflammatory_Pathology]][[Category:Arterial_Pathology]] | [[Category:Cardiovascular_System_-_Vascular_Pathology]][[Category:Cardiovascular_System_-_Inflammatory_Pathology]][[Category:Arterial_Pathology]] | ||
− | [[Category: | + | [[Category:Coagulation Defects]][[Category:Vascular Diseases - Dog]][[Category:Lymphoreticular and Haematopoietic Diseases - Dog]][[Category:Vascular Diseases - Cat]] |
+ | [[Category:Expert_Review]] | ||
+ | [[Category:Cardiology Section]] |
Latest revision as of 04:18, 14 October 2014
Also known as: DIC — Consumptive Coagulopathy
Introduction
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.
- 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 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.
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.
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.
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