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Spring 1999 Newsletter

Histopathology Service
Caprine Arthritis Enchephalitis Virus
Pythiosis in Dogs
Disseminated Intravascular Coagulation
Infectious Pancreatic Necrosis Virus
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Disseminated Intravascular Coagulation

            Disseminated Intravascular Coagulation (DIC) is a syndrome characterized by massive activation and consumption of coagulation proteins, fibrinolytic proteins and platelets.  It is not a primary disease, but a disorder secondary to numerous triggering events such as bacterial, viral, rickettsial, protozoal, parasitic diseases, heat stroke, burns, neoplasia and severe trauma.  In 41 cases of disseminated intravascular coagulation, 39% were secondary to malignancy, 30% from pancreatitis, 4% from sepsis, 14% from chronic active hepatitis and 12% secondary to heat stroke.  Disseminated intravascular coagulation can be traced to platelet activation and/or the release of thromboplastins into the circulation from tissue damage from various conditions listed above.  It can be acute, subacute or chronic and can be localized or generalized.  Its severity is related to the rate of release of thromboplastin, the duration of exposure to the causative agent, the ability of the liver to replace consumed coagulation factors, and the ability of the bone marrow to restore platelets.

            Tissue necrosis, inflammation, red cell or platelet damage, or endothelial damage induced by antigen-antibody or endotoxin initiates the coagulation process which ultimately forms a clot.  Simultaneously, the fibrinolytic system is also activated.  Plasmin, the active protease in fibrinolysis, degrades fibrinogen and fibrin, producing fibrin degradation products which in turn prevent fibrin polymerization.  Plasmin can also degrade coagulation factors.  Thus, the bleeding tendency in disseminated intravascular coagulation patients is a consequence of the depletion of coagulation factors and platelets and the anticoagulant properties of fibrin degradation products.

            Coagulation disorders are characterized by spontaneous hemorrhage and/or excessive bleeding after surgery or trauma.  Hemorrhage into the central nervous system may cause acute onset of neurological dysfunction or sudden death.  Bleeding in association with disseminated intravascular coagulation is usually severe and occurs from mucosal surfaces and into body cavities.  In addition, signs of the underlying disease are usually present.  Other signs include shock, petechiae and ecchymoses of the skin and mucous membranes.  The organ or organs involved with their accompanying signs and clinical effects must also be taken into consideration.

            Laboratory diagnosis is usually based on the triad of prolonged prothrombin time (PT), thrombocytopenia, and hypofibrino-genemia.  The finding of fibrin-fibrinogenemia degradation products (FDP's), schistocytes (fragmented erythrocytes) in blood smears, and decreased concentrations of coagulation factors (factors V and VIII and antithrombin III) aid in the diagnosis.  Also APTT and thrombin clotting time (TCT) are prolonged.

            Therapy should be approached in a logical and sequential fashion.  The most important measure involves removal of the inciting cause.  When this is not possible, specific treatment may be indicated.  Fluid therapy is used to correct hypovolemia; prevent or alleviate vascular stasis; and dilution of thrombin, FDP's and activators of fibrinolysis.  Drugs for inhibiting coagulation are indicated if the patient manifests direct evidence of bleeding, thrombosis, or organ dysfunction.  Heparin potentiates the action of plasma antithrombin III.  When patients with DIC bleed, replacement of some or all blood constituents is indicated to replenish depleted coagulation factors and platelets.  Plasma infusion is preferred, but whole blood may be given if red cell infusion is necessary.  The infusion of red cells carries the risk of hemolysis and exacerbation of DIC.

            Normalization of the screening coagulogram (PT, APTT, and FDP's) usually denotes successful therapy.  The return of the normal fibrinogen concentration is a reliable long-term indicator of heparin therapy.


- by Arthur Newman, ECFVG

- edited by VictoriaOwiredu-Laast, DVM





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