NAVLE Multisystemic

Feline Disseminated Intravascular Coagulation (DIC) – NAVLE Study Guide

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...

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.

High-YieldOn the NAVLE, remember that DIC in cats primarily manifests as thrombosis rather than hemorrhage. Only 15% of cats with DIC exhibit bleeding, compared to over 75% of dogs. The 93% mortality rate makes early recognition and treatment of underlying disease critical.
Inhibitor Mechanism of Dysfunction in DIC
Antithrombin (AT) Consumed forming TAT complexes; degraded by neutrophil elastases; decreased hepatic synthesis (less pronounced in cats vs dogs)
Protein C Decreased activation due to downregulated thrombomodulin; histones bind and inhibit protein C
Protein S Bound by C4-binding protein (acute phase reactant); decreases protein C and TFPI activity
TFPI Cleaved by neutrophil elastases; overwhelmed by excess TF-FVIIa complex formation

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.

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