Difference between revisions of "Disseminated Intravascular Coagulation"

Revision as of 15:11, 1 July 2010

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.

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-{{OpenPagesTop}}
+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.
-Also known as: '''''DIC — Consumptive Coagulopathy'''''
-==Introduction==
+There are multiple aetiologies for DIC, however, once the cascadeis under way the disease process is essentially the same.  Causes include:
-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 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.
+*Tissue trauma E.g. burns.
 *Liver disease.
-*[[Administering_a_Blood_Transfusion#Adverse_Reactions|Transfusion reactions]].
+*Transfusion reaction.
 *Neoplasia.
+*Viral haemorrhagic fevers.
 *Certain snake venoms.
-*Acute haemolytic crises.
-*Infections (viral, bacterial, protozoal) and post-infectious immunologic reactions.
-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.
+''Pathophysiology'':
-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 [[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.
+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.
-==Clinical Symptoms==
+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.
-These are noted due to spontaneous primary bleeding, including petechiae, ecchymoses, mucosal bleeding or secondary bleeding into body cavities e.g. [[Haemoabdomen|haemoabdomen]].
-[[:Category:Altered Ventricular Impulse Formations|Ventricular arrythmias]] may also be present due to myocardial hypoxia or thrombosis.
-==Laboratory Tests==
+DIC has a poor prognosis with a high mortality rate.
-===Blood Smear===
-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|neutrophilia]] with a left shift and thrombocytopaenia will be present. Schistocytes may also be seen due to haemolysis.
-===Biochemistry===
-Can reveal an [[Azotaemia|azotaemia]] and hyperphosphataemia, increased [[Liver - Anatomy & Physiology|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===
+''Treatment'':
-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|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 components must be replaced via [[:Category:Transfusion Medicine|transfusion]] with fresh frozen [[Plasma|plasma]] to provide clotting factors and platelets.
-==Prognosis==
-DIC has a poor prognosis with a high mortality rate.
+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.
-{{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]
-}}
+* 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 - Pathology|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.
-{{review}}
-{{OpenPages}}
 [[Category:Cardiovascular_System_-_Vascular_Pathology]][[Category:Cardiovascular_System_-_Inflammatory_Pathology]][[Category:Arterial_Pathology]]
-[[Category:Coagulation Defects]][[Category:Vascular Diseases - Dog]][[Category:Lymphoreticular and Haematopoietic Diseases - Dog]][[Category:Vascular Diseases - Cat]]
+[[Category:To_Do_-_Cardiovascular]]
-[[Category:Expert_Review]]
-[[Category:Cardiology Section]]

Difference between revisions of "Disseminated Intravascular Coagulation"

Revision as of 15:11, 1 July 2010

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