Disseminated Intravascular Coagulation
Etiology and Pathogenesis
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DIC is not a specific disease but rather a complex syndrome resulting from excessive intravascular coagulation that leads to microthrombosis in organs and paradoxical bleeding.
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It is caused by endothelial damage, platelet activation, and the release of tissue "procoagulants" that initiate the coagulation cascade.
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Endothelial damage: Often due to electrocution, heatstroke, or sepsis.
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Platelet activation: Triggered mainly by viral infections (e.g., FIP in cats).
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Tissue procoagulants: Released in cases of trauma, hemolysis, pancreatitis, bacterial infections, and some cancers (e.g., hemangiosarcoma in dogs).
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The condition leads to:
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Intravascular coagulation, thrombocytopenia, fibrinolysis, and organ failure.
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Fragmentation of red blood cells (RBCs) due to microthrombi in vessels (schistocytes).
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Clinical Features
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Acute DIC: More common in dogs, presents with spontaneous bleeding (e.g., petechiae, ecchymosis), organ dysfunction, and anemia. It may be triggered by acute events such as heatstroke, electrocution, or pancreatitis. Rare in cats.
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Chronic DIC: Often associated with malignancy (e.g., hemangiosarcoma), chronic disorders, or decompensated disease processes.
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Signs:
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Bleeding (spontaneous, mucosal, or body cavity bleeding).
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Hemolysis (anemia, hemoglobinemia, RBC fragments, schistocytes).
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Thrombocytopenia and neutrophilia (often with a left shift).
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Organ dysfunction, often manifesting as pulmonary or renal issues.
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Diagnosis:
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Hemostatic abnormalities such as thrombocytopenia, prolonged OSPT or APTT, low fibrinogen, positive FDP test, and decreased AT III levels.
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Enhanced fibrinolysis with decreased plasminogen activity or abnormal clot lysis tests.
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Diagnosis
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Clinical signs: Presence of bleeding, organ failure, and hematologic abnormalities.
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Laboratory tests:
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Thrombocytopenia
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Prolonged OSPT/APTT
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Low fibrinogen levels
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Positive FDP test
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Decreased AT III concentration
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Schistocytes in blood smear.
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DIC Diagnosis: Four or more hemostatic abnormalities, especially in the presence of schistocytes.
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Treatment
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General Approach: Immediate treatment is critical. The main goals are to address the underlying cause, halt the intravascular coagulation, and maintain organ perfusion.
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Therapeutic Strategies:
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Removal or treatment of the underlying cause (e.g., surgery for hemangiosarcoma, antimicrobial treatment for sepsis, immunosuppressive therapy for immune-mediated diseases).
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Heparin: Used to halt coagulation; works by enhancing antithrombin III (AT III) activity. Doses range from low to high (e.g., 5–1000 IU/kg SQ or IV every 8 hours).
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Blood Products: Whole fresh blood or fresh-frozen plasma to provide anticoagulant factors and support AT III levels.
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Fluid Therapy: Crystalloids or plasma expanders (e.g., dextran) to dilute clotting and fibrinolytic factors, improve microcirculation, and maintain parenchymal organ perfusion.
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Supportive Care: Oxygenation, correcting acidosis, managing arrhythmias, and preventing secondary infections (e.g., bacterial infections due to compromised gastrointestinal mucosa).
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Prognosis
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The prognosis is guarded and depends on the underlying cause, the extent of organ damage, and the rapidity of treatment.
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Dogs with DIC are at high risk for death from pulmonary or renal dysfunction, with DIC lungs being a common cause of death.
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Survival: Improved with prompt use of heparin and blood products, though recovery can be prolonged and varies depending on the underlying condition.
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Prevention
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Prevention of DIC:
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Early recognition and management of underlying diseases (e.g., infection, cancer, trauma).
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Supportive care and monitoring in high-risk patients.
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Management of conditions like heatstroke, pancreatitis, and infections before they lead to DIC.
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