Feline Disseminated Intravascular Coagulation (DIC) – NAVLE Study Guide

Overview and Clinical Importance

Disseminated intravascular coagulation (DIC) is a complex, life-threatening syndrome characterized by systemic activation of coagulation pathways, leading to widespread microvascular thrombosis and subsequent consumption of platelets and clotting factors. In cats, DIC is always secondary to another primary disease and carries a grave prognosis, with survival rates as low as 7% in retrospective studies.

DIC should be conceptualized as a continuum rather than a single event. It begins with a non-overt (compensated) phase where coagulation is activated but controlled by inhibitors, and may progress to an overt (decompensated) phase characterized by uncontrolled thrombosis and eventual hemorrhage. Unlike dogs, cats with DIC rarely present with overt bleeding (only 15% of cases), making diagnosis more challenging.

Pathophysiology

The DIC Continuum

DIC develops through distinct phases that reflect the balance between procoagulant and anticoagulant forces. The process begins with an initiating trigger from the primary disease, followed by amplification, progression, and ultimately dissemination throughout the vasculature.

Phase 1: Initiation of Coagulation

The primary mechanism of DIC initiation is excessive exposure of tissue factor (TF), which activates the extrinsic coagulation pathway. Sources of tissue factor in cats include:

• Neoplastic cells: Constitutive expression of TF on tumor cells and shed extracellular vesicles
• Inflammatory cytokines: Upregulate TF expression on monocytes and endothelial cells
• Endothelial damage: Exposes subendothelial TF to circulating blood
• Nuclear material (DAMPs): Cell-free DNA and histones from NETosis activate Factor XII

Phase 2: Amplification

Thrombin plays a central role in amplifying coagulation through positive feedback mechanisms. Once generated, thrombin activates Factors V, VIII, and XI, leading to exponential thrombin generation (the "thrombin burst"). Activated platelets provide phosphatidylserine-rich surfaces that accelerate coagulation factor assembly.

Phase 3: Progression and Loss of Inhibition

As DIC progresses from non-overt to overt, natural anticoagulant mechanisms become overwhelmed or downregulated:

Phase 4: Fibrinolysis Balance

The balance between fibrinolysis and antifibrinolysis determines clinical phenotype. In cats (similar to humans), antifibrinolytic mechanisms tend to dominate, leading to a primarily thrombotic phenotype. This is mediated by increased plasminogen activator inhibitor-1 (PAI-1) and the antifibrinolytic effects of histones and polyphosphates. Dogs, in contrast, have robust fibrinolysis with high tissue plasminogen activator (tPA) activity, explaining their hemorrhagic phenotype.

Underlying Diseases Associated with Feline DIC

DIC is NEVER a primary disease and always occurs secondary to another condition. Identifying and treating the underlying cause is the cornerstone of DIC management.

Clinical Presentation

Thrombotic Phenotype (Most Common in Cats)

Because cats tend toward a thrombotic rather than hemorrhagic phenotype, clinical signs are often subtle and attributable to microvascular thrombosis and end-organ damage:

• Respiratory: Dyspnea, tachypnea (pulmonary thromboembolism, ventilation-perfusion mismatch)
• Renal: Acute kidney injury, oliguria, azotemia
• Hepatic: Elevated liver enzymes, hyperbilirubinemia
• Neurologic: Altered mentation, seizures (rare)
• Cardiovascular: Poor perfusion, hypotension, weak pulses

Hemorrhagic Phenotype (Uncommon in Cats)

Only approximately 15% of cats with DIC exhibit clinical hemorrhage. When present, signs include:

• Petechiae and ecchymoses on gums, pinnae, or ventral abdomen
• Prolonged bleeding from venipuncture sites
• Epistaxis, hematuria, melena (rare)
• Body cavity hemorrhage

Diagnosis

No single test is diagnostic for DIC. Diagnosis requires a combination of: (1) identification of an underlying predisposing disease, (2) clinical signs consistent with DIC, and (3) three or more abnormal coagulation test results.

Laboratory Testing

Diagnostic Criteria for Feline DIC

A diagnosis of DIC requires: (1) An identified predisposing condition, AND (2) three or more of the following abnormalities:

• Prolonged PT (greater than 25% above control)
• Prolonged aPTT (greater than 25% above control)
• Thrombocytopenia
• Low fibrinogen concentration
• Elevated FDPs or D-dimer
• Decreased antithrombin activity

"Cats Are Thrombotic, Dogs Are Dripping" Cats = Clot (thrombotic phenotype) Antithrombin often normal in cats Thrombocytopenia variable/unreliable Schistocytes rare (only 8%) Dogs = Dripping (hemorrhagic) Obvious bleeding (75%+ of dogs) Great sensitivity: AT low, schistocytes present Severe thrombocytopenia common

Treatment

The cornerstone of DIC treatment is identification and treatment of the underlying disease. Without addressing the primary trigger, DIC will persist or worsen. Supportive care aims to restore tissue perfusion, provide hemostatic support, and prevent further organ damage.

Prognosis

Prognosis for feline DIC is grave. In a retrospective study of 46 cats with DIC:

• Survival rate: Only 7% (3 of 46 cats survived)
• Mortality: 93% died or were euthanized
• Prognostic indicator: Prolonged PT was significantly associated with non-survival
• Age range: 7 weeks to 17 years (median 9 years)

Factors that did NOT correlate with outcome included signalment, specific underlying disease, hemorrhage, aPTT, fibrinogen, FDPs, platelet count, blood transfusion, or heparin therapy. The only identified negative prognostic factor was more prolonged PT.