Dilution of blood samples with all HES solutions resulted in changes in viscoelastic coagulation and platelet function that did not appear to be attributable to dilution alone. In vivo evaluations are necessary to understand the clinical impact of these in vitro changes.

Viscoelastic coagulation monitoring with strong coagulation activators may be used to monitor treatment with dalteparin in healthy dogs.

Background: Thrombocytopenia in dogs is common in critical care medicine, but availability of fresh platelet concentrates in veterinary medicine can be limiting. Lyophilized platelets have long shelf-lives and can be easily transported, stored, and administered in various settings. Objective: To evaluate the efficacy and safety of a novel trehalose-stabilized canine lyophilized platelet product in thrombocytopenic dogs with clinically-evident bleeding. Animals: Eighty-eight dogs with platelet counts <50 × 10 3 /μL and a standardized bleeding assessment tool (DOGiBAT) score ≥2. Methods: Multicenter, randomized, non-blinded, non-inferiority clinical trial comparing dimethyl sulfoxide (DMSO)-stabilized cryopreserved platelet concentrates (CPP) with trehalose-stabilized lyophilized platelets (LP) for control of bleeding in thrombocytopenic dogs. Dogs were randomized to receive 3 × 10 9 platelets/kg of LP or CPP. Primary outcome measures were change in DOGiBAT score, platelet count, need for additional red cell transfusion and all-cause mortality.

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Objective To describe the successful case management of an extradural hematoma secondary to anticoagulant rodenticide toxicity causing spinal compression and paraplegia. Case Summary A 3‐month‐old, female intact, mixed breed dog was presented for a 12‐hour history of paraplegia. CBC and biochemistry results were unremarkable, and a coagulation panel revealed prolonged prothrombin time with normal activated partial thromboplastin time. Magnetic resonance imaging revealed an extradural compressive lesion within the vertebral canal extending from T6 to T11, most consistent with an extradural hematoma. Further coagulation testing revealed a coagulopathy caused by vitamin K1 deficiency and confirmed exposure to the anticoagulant rodenticide, diphacinone. The dog was medically managed with fresh frozen plasma, aminocaproic acid, and oral vitamin K1 therapy. A right‐sided T6 to T11 hemilaminectomy was later performed for removal of the extradural hematoma and spinal decompression. The dog's neurological status gradually improved postoperatively and, at the time of discharge, was nonambulatory paraparetic with voluntary micturition. Four weeks postoperatively, the dog had normal prothrombin and activated partial thromboplastin times and was nonambulatory paraparetic with strong motor function. New or Unique Information Provided This is the first reported case of a dog with an extradural hematoma secondary to anticoagulant rodenticide causing spinal cord compression and neurological deficits. Surgical management of this case was successful and resulted in improvement of neurological signs. Extradural hematoma should be considered as a potential location of bleeding in rodenticide toxicity as well as a differential diagnosis in patients with neurological deficits.