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Disseminated Intravascular Coagulation (DIC) in Dogs & Cats

Disseminated Intravascular Coagulation (DIC) is a critical hemostatic disorder in dogs and cats that occurs exclusively as a complication of an underlying disease process. It is defined by uncontrolled, systemic activation of coagulation pathways leading to widespread microthrombosis, consumption of clotting factors, and ultimately, a paradoxical bleeding tendency. The condition represents a continuum—from subtle, chronic forms with minimal clinical evidence to acute, fulminant presentations characterized by severe hemorrhage and multiorgan dysfunction. Common triggers include sepsis, immune-mediated hemolytic anemia, severe trauma, heat stroke, pancreatitis, and certain neoplasms. Because of its complex pathophysiology, rapid evolution, and poor prognosis, early recognition of clinical signs and interpretation of coagulation profiles are essential for diagnosis and management.

DIC NAVLE Review


Overview

Disseminated Intravascular Coagulation (DIC) is an acquired, severe hemostatic disturbance that always occurs secondary to another underlying disease. It involves dysregulated activation of coagulation and fibrinolysis, resulting in widespread microthrombosis, consumption of platelets and coagulation factors, and paradoxically, hemorrhage. Recognizing DIC promptly is vital due to its high morbidity and mortality in veterinary patients.


Etiology & Predisposing Conditions

DIC is never primary; common initiating triggers in dogs and cats include:

  • Systemic inflammation (e.g. sepsis, pancreatitis)

  • Massive endothelial injury or exposure of tissue factor (e.g. from neoplasia, trauma)

  • Immune-mediated hemolytic anemia (IMHA)

  • Heat stroke, severe infection, endotoxemia


Pathophysiology

The disease begins with excessive generation of thrombin and fibrin, often via the extrinsic or intrinsic coagulation pathways, frequently triggered by tissue factor from damaged endothelium or activated monocytes. Simultaneously, fibrinolysis is activated, but as coagulation continues unchecked, platelets, fibrinogen, and clotting factors become depleted. Microthrombi occlude small vessels, causing organ dysfunction; when consumptive coagulopathy progresses, hemorrhagic tendencies emerge.


Clinical Presentation

Clinical signs vary depending on whether DIC is evolving slowly (chronic/non-overt) or acutely severe:

  • Slow/non-overt DIC: May have few external signs, possibly thrombotic events (e.g. pulmonary emboli), mild thrombocytopenia.

  • Acute/rapid DIC: Bleeding from venipuncture/injection sites, mucosal bleeding, ecchymoses, GI hemorrhage, epistaxis, hematuria; signs of organ failure (kidney, liver, lungs) due to microvascular thrombosis.

Cats with DIC often have less overt bleeding; their presentation may be dominated by the primary disease process.


Diagnostics & Interpretation

No single test defines DIC. Diagnosis is based on history, clinical signs, and multiple laboratory abnormalities. Key diagnostic elements include:


Test

What is expected in DIC

Platelet count

Thrombocytopenia (often marked)

Prothrombin Time (PT) / Activated Partial Thromboplastin Time (aPTT)

Prolongation due to factor consumption

Fibrinogen level

Reduced in acute-severe DIC; may be normal or elevated in early or chronic stages due to acute-phase reaction

D-dimer / Fibrin Degradation Products (FDPs)

Increased; reflects fibrin formation and breakdown

Blood smear

Schistocytes in some cases (evidence of microangiopathic hemolysis)



Multiple abnormal lab values (often ≥3) plus compatible clinical picture are required for diagnosis. Serial testing helpful to detect trends.


Treatment

Management is primarily supportive and aims at:

  1. Treating the underlying cause (e.g. infection, immune disease, neoplasia). Without this, DIC persists.

  2. Restoring and preserving organ perfusion: aggressive fluid therapy to correct hypovolemia and maintain microcirculation.

  3. Replacing consumed hemostatic components: fresh frozen plasma, whole blood if anemia or coagulopathy severe.

  4. Balancing coagulation vs bleeding: In slowly evolving or thrombosis-dominant cases, cautious anticoagulants (heparin) may be considered; in overt bleeding, supportive transfusion and factor replacement take priority.



Prognosis & NAVLE-Relevant Highlights
  • Prognosis is guarded to poor, depending heavily on severity, rapidity of onset, degree of hemorrhage, organ dysfunction, and whether the primary disease is reversible.

  • Cats less often show severe overt bleeding; often suffer from primary disease effects.

  • For exam takers: know that DIC is always secondary; key lab findings include thrombocytopenia, prolonged PT/aPTT, decreased fibrinogen, elevated D-dimer/FDPs; treatment is supportive + address trigger; anticoagulation only if indicated.


References

Merck Veterinary Manual; Veterinary Partner / VIN; EClinPath hemostasis resources; Bruchim et al. “Disseminated Intravascular Coagulation in Dogs and Cats”, PubMed; Research compiled in veterinary hemostasis literature.

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