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Updated: Jun 4, 2026
Ferric Chloride-induced Canine Carotid Artery Thrombosis: A Large Animal Model of Vascular Injury
Published on: September 7, 2018
Identification of hypercoagulability in dogs with primary immune-mediated hemolytic anemia by means of
Renee K Fenty1, Armelle M Delaforcade, Scott E Shaw
1Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University, North Grafton, MA 01536, USA. r.fenty@vetspecialistsvalley.com
Objective:
To evaluate whole blood hemostasis by means of thromboelastography in dogs with primary immune-mediated hemolytic anemia (IMHA) to determine whether these dogs had evidence of hypercoagulability prior to the administration of immunosuppressant medications, blood transfusion products, or anticoagulant agents.
Design:
Evaluation study.
Animals:
11 client-owned dogs admitted to a teaching hospital for management of primary IMHA and 20 clinically normal dogs.
Procedures:
Citrated whole blood samples were obtained from all dogs for performance of kaolin-activated thromboelastography. Citrated plasma was harvested from blood samples of dogs with IMHA for plasma-based coagulation testing, including activated partial thromboplastin time, prothrombin time, D-dimer concentration, fibrinogen concentration, and antithrombin activity.
Results:
Compared with control dogs, dogs with primary IMHA had evidence of hypercoagulability as indicated by a significantly lower median (range) clot formation time (0.8 seconds [0.8 to 2.0 seconds] vs 1.9 seconds [1.3 to 3.8 seconds]), higher median angle (76.1° [59.2° to 84.6°] vs 64.0° [45.4° to 71.0°]), higher median maximum amplitude (75.9 mm [66.3 to 86.3 mm] vs 55.7 mm [49.9 to 63.6 mm]), and higher median clot strength (15,000 dyne/cm(2) [9,900 to 31,400 dyne/cm(2)] vs 6,100 dyne/cm(2) [4,900 to 8,700 dyne/cm(2)]).
Conclusions And Clinical Relevance:
Dogs with primary IMHA had hypercoagulability as demonstrated by thromboelastography at the time of initial diagnosis and prior to treatment. Such hypercoagulability may be a precursor to clinically evident thrombosis as a complication of the disease process.
