Characterization of thrombelastography over time in dogs with hyperadrenocorticism

• Published in: The veterinary journal (1997) Vol. 197; no. 3; pp. 675 - 681
• Main Authors: Kol, A., Nelson, R.W., Gosselin, R.C., Borjesson, D.L.
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.09.2013
• Subjects: Adrenocortical Hyperfunction - blood; Adrenocortical Hyperfunction - veterinary; Animals; blood; blood coagulation; Canine; Coagulation; Cohort Studies; Dog Diseases - blood; Dogs; fibrinogen; glucocorticoids; Hyperadrenocorticism; morbidity; mortality; secretion; Thrombelastography; Thrombelastography - veterinary; Thrombosis; Hyperadrenocorticism; Thrombelastography; Thrombosis; Coagulation; Canine
• ISSN: 1090-0233; 1532-2971
• DOI: 10.1016/j.tvjl.2013.05.047

Canine hyperadrenocorticism (HAC) is a common endocrinopathy often associated with hypercoagulability, thrombosis and thromboembolism and it can contribute to increased morbidity and mortality. The condition results in increased, unregulated secretion of glucocorticoids (GCs). While prospective identification of hypercoagulability is challenging, thrombelastography (TEG) is a diagnostic tool that enables the detection of hypercoagulability in a clinical setting. The objective of this prospective cohort study was to serially assess coagulation in dogs with HAC using TEG to test the hypothesis that dogs with HAC have increased TEG maximal amplitude (MA) and that the MA would normalize once clinical control was achieved. Twenty-three dogs with naturally occurring HAC were enrolled and hemostatic (including TEG, platelet function, thrombin–antithrombin complexes and coagulation panel) and hematological variables were measured at presentation. TEG was serially monitored until clinical resolution of HAC was attained. At presentation, most dogs with HAC had increased MA values, increased thrombin–antithrombin complexes and many were hyperfibrinogenemic. Platelet function analyzer-100 (PFA-100) closure times were significantly prolonged. TEG tracings did not normalize in either medically- or surgically-managed dogs, but fibrinogen concentrations decreased. It seems that dogs with HAC have a complex coagulopathy in which hypercoagulability and platelet hyporeactivity or dysfunction might occur simultaneously. As TEG tracings did not normalize in well-controlled dogs, it is unlikely that increased blood GCs are solely responsible for TEG alterations seen in dogs with HAC.