White blood cells (WBCs) and storage period are the main factors of transfusion reactions. In the present study, cytokine/chemokine concentrations after leukoreduction (LR) and irradiation (IR) in stored canine whole blood were measured. Red blood cell storage lesion caused by IR and LR were also compared. Blood samples from 10 healthy Beagles were divided into four groups (no treatment, LR-, IR-, and LR + IR-treated). Leukocytes were removed by filtration in the LR group and gamma radiation (25 Gy) was applied in the IR group. Immunologic factors (WBCs, interleukin-6 [IL-6], C-X-C motif chemokine ligand 8 [CXCL-8], and tumor necrosis factor-alpha) and storage lesion factors (blood pH, potassium, and hemolysis) were evaluated on storage days 0, 7, 14, 21, and 28. Compared to the treated groups, IL-6 and CXCL-8 concentrations during storage were significantly higher in the control (no treatment) group. LR did not show changes in cytokine/chemokine concentrations, and storage lesion presence was relatively mild. IR significantly increased CXCL-8 after 14 days of storage, but IR of leukoreduced blood did not increase CXCL-8 during 28 days of storage. Storage lesions such as hemolysis, increased potassium, and low pH were observed 7 days after IR and storage of blood, regardless of LR. IR of leukoreduced blood is beneficial to avoid immune reactions; however, storage lesions should be considered upon storage.

Background The chromogenic anti‐Xa assay, the gold standard for monitoring the anti‐Xa effect of rivaroxaban, is not available as a cage‐side diagnostic test for use in a clinical setting. Hypothesis/Objectives To evaluate clinical modalities for measuring the anticoagulant effects of rivaroxaban using a point‐of‐care prothrombin time (PT) and thromboelastography (TEG). Animals Six healthy Beagle dogs. Methods Prospective, experimental study. Four different doses of rivaroxaban (0.5, 1, 2, and 4 mg/kg) were administered PO to dogs. Single PO and 3 consecutive dosing regimens also were assessed. Plasma rivaroxaban concentration was determined using a chromogenic anti‐Xa assay, point‐of‐care PT, and TEG analysis with 4 activators (RapidTEG, 1 : 100 tissue factor [TF100], 1 : 3700 tissue factor [TF3700], and kaolin), and results were compared. Spearman correlation coefficients were calculated between ratios (peak to baseline PT; peak reaction time [R] of TEG to baseline [R] of TEG) and anti‐Xa concentration. Results Anti‐Xa concentration had a significant correlation with point‐of‐care PT (R = 0.82, P < .001) and RapidTEG‐TEG, TF100‐TEG, and TF3700‐TEG (R = 0.76, P < .001; R = 0.82, P < .001; and R = 0.83, P < .001, respectively). Conclusions and Clinical Importance Overall, a 1.5‐1.9 × delay in PT and R values of TEG 3 hours after rivaroxaban administration is required to achieve therapeutic anti‐Xa concentrations of rivaroxaban in canine plasma. The R values of TEG, specifically using tissue factors (RapidTEG, TF100, TF3700) and point‐of‐care PT for rivaroxaban can be used practically for therapeutic monitoring of rivaroxaban in dogs.

Hydroxyethyl starches (HES) are commonly used synthetic colloidal solution in veterinary medicine. Despite of possible adverse effect to kidney injury in human, there is no report about nephrotoxic effects of HES in dogs. HES was administered to a Golden retriever (4-year-old, intact male) with ascites in order to increase plasma osmolality. Initially, the dog was mild azotemic, however, kidney function was rapidly deteriorated after several days of HES administration. Finally, histopathological examination revealed remarkable osmotic nephrosis. In the case reported herein, acute kidney injury was remarkably developed after HES administration. Clinical and histopathologic findings of acute kidney injury support nephrotoxic effects of HES to a dog.

No abstract

Acute lymphocytic leukemia (ALL) is uncommon lymphoid malignancy in dogs, and its diagnosis is challenging. A 14-year-old spayed female mixed breed dog was transferred to a veterinary medical teaching hospital for an immediate blood transfusion. The dog showed lethargy, pale mucous membranes, and a weak femoral pulse. Complete blood count revealed non-regenerative anemia and severe leukopenia with thrombocytopenia. ALL was tentatively diagnosed based on the predominance of immature lymphoblasts on blood film examination. For confirmation of lymphoid malignancy, PCR for antigen receptor rearrangement (PARR) on a peripheral blood sample and flow cytometry analysis were performed after blood transfusion. Flow cytometry analysis revealed that lymphocyte subsets were of normal composition, but PARR detected a T-cell malignancy. The dog was diagnosed with ALL and survived 1 wk after diagnosis. In conclusion, after blood transfusion, flow cytometry was not a reliable diagnostic method for an ALL dog, whereas PARR could detect lymphoid malignancy. Our results suggest that PARR should be the first-line diagnostic tool to detect canine lymphoid malignancy after a blood transfusion.