BackgroundCyclosporine increases thromboxane synthesis in dogs, potentially increasing the thrombogenic properties of platelets.Hypothesis/ObjectivesOur hypothesis was that the concurrent administration of low‐dose aspirin and cyclosporine would inhibit cyclosporine‐associated thromboxane synthesis without altering the antiplatelet effects of aspirin. The objective was to determine the effects of cyclosporine and aspirin on primary hemostasis.AnimalsSeven healthy dogs.MethodsA randomized, crossover study utilized turbidimetric aggregometry and a platelet function analyzer to evaluate platelet function during the administration of low‐dose aspirin (1 mg/kg PO q24h), high‐dose aspirin (10 mg/kg PO q12h), cyclosporine (10 mg/kg PO q12h), and combined low‐dose aspirin and cyclosporine. The urine 11‐dehydro‐thromboxane‐B2 (11‐dTXB 2)‐to‐creatinine ratio also was determined.ResultsOn days 3 and 7 of administration, there was no difference in the aggregometry amplitude or the platelet function analyzer closure time between the low‐dose aspirin group and the combined low‐dose aspirin and cyclosporine group. On day 7, there was a significant difference in amplitude and closure time between the cyclosporine group and the combined low‐dose aspirin and cyclosporine group. High‐dose aspirin consistently inhibited platelet function. On both days, there was a significant difference in the urinary 11‐dTXB 2‐to‐creatinine ratio between the cyclosporine group and the combined low‐dose aspirin and cyclosporine group. There was no difference in the urinary 11‐dTXB 2‐to‐creatinine ratio among the low‐dose aspirin, high‐dose aspirin, and combined low‐dose aspirin and cyclosporine groups.Conclusions and Clinical ImportanceLow‐dose aspirin inhibits cyclosporine‐induced thromboxane synthesis, and concurrent use of these medications does not alter the antiplatelet effects of aspirin.

A 12-year-old male neutered Bichon Frise presented to the Emergency Department for stupor and bradycardia after ingestion of chocolate covered 450 mg (90 mg/kg) tetrahydrocannabinol. The patient was hospitalized for supportive care, IV fluid therapy and monitoring in the intensive care unit. During hospitalization the patient became comatose and bradypneic. Treatment with intravenous lipid emulsion (ILE) therapy was instituted to accelerate toxin elimination, reduce the risk of complications related to progressive obtundation and shorten hospitalization time. Five hours after infusion, the patient developed severe respiratory distress and was ultimately euthanized. Post-mortem histologic evaluation of lung revealed severe pulmonary edema consistent with acute respiratory distress syndrome. There are infrequent reports of adverse effects associated with ILE therapy for toxicosis in veterinary medicine despite reports of complications such as acute respiratory distress syndrome in human literature. The purpose of this report is to describe the potential for a severe adverse event after treatment of a toxicosis with ILE therapy.

This hypothesis-generating study found irradiation and storage significantly altered in vitro properties of pRBC. The magnitude of these differences was small and the clinical impact of irradiation on pRBC may be negligible.

OBJECTIVE To determine the pharmacokinetics and efficacy of trazodone following rectal administration of a single dose to healthy dogs. ANIMALS 6 healthy adult dogs. PROCEDURES Each dog received a single dose of trazodone (approx 8 mg/kg) per rectum. Trazodone tablets were crushed into a powder, mixed with 5 mL of tap water, and injected into the rectum via a red rubber catheter. Sedation scores were assigned, and blood samples were collected for determination of plasma trazodone concentration at predetermined times before and after drug administration. Pharmacokinetic parameters were estimated by noncompartmental analysis. RESULTS Plasma trazodone concentration remained below the detection limit for 1 dog even though it became moderately sedate. Median (interquartile [25th to 75th percentile] range [IQR]) maximum plasma trazodone concentration and volume of distribution and clearance corrected for bioavailability were 1.00 μg/mL (0.66 to 1.40 μg/mL), 10.3 L/kg (7.37 to 14.4 L/kg), and 639 mL/kg/h (594 to 719 mL/kg/h), respectively. Median time to maximum plasma trazodone concentration and elimination half-life were 15 minutes (range, 15 to 30 minutes) and 12 hours (IQR, 7.99 to 12.7 hours), respectively. All dogs became mildly or moderately sedate, and the extent of sedation was maximal at a median of 30 minutes (IQR, 30 to 60 minutes) after trazodone administration. No adverse effects were observed. CONCLUSIONS AND CLINICAL RELEVANCE Rectal administration of trazodone may be a viable option for sedation and treatment of anxiety in dogs for which administration of sedatives and anxiolytics by other routes is contraindicated. Further research is necessary to better elucidate the pharmacokinetics and efficacy of trazodone following rectal administration and determine optimal dosing.

Objective: To describe the successful treatment of lethal dose 5-fluorouracil (5-FU) toxicosis using hemodialysis.Case Summary: A 4-month-old intact female Golden Retriever was presented to the emergency department after ingesting 20 g of 5% 5-FU cream. The puppy developed refractory seizures and became comatose with uncontrolled tonic-clonic convulsions.Because of the low molecular weight and minimal protein binding of 5-FU, a single hemodialysis treatment was employed for detoxification. The puppy improved clinically posttreatment and was successfully discharged 3 days after admission.Postingestion leukopenia and neutropenia occurred but were responsive to treatment with filgrastim. The puppy is neurologically normal and has no lasting effects 1 year postingestion.