Search

Objectives: Acute kidney injury (AKI) is a well‐known but poorly documented adverse effect of non‐steroidal anti‐inflammatory drugs (NSAIDs) in cats. We aimed to describe instances of NSAID‐associated AKI in cats and survey Australian veterinarians on NSAID use in acute settings. Methods: Medical records of cats that developed an AKI subsequent to the administration of meloxicam were obtained by searching the databases of seven practices in Queensland, as well as by contemporaneously contacting select veterinary colleagues of the authors in both general and specialist small animal practice. An online questionnaire was created for the survey, and the URL distributed to Australian practitioners. Results: A total of 18 cases were retrieved, all of which received injectable meloxicam. The indication(s) for its use and the dosage prescribed were within the manufacturer's recommendations for Australian veterinarians. The majority of cases (13/18 cats) received the label dose of 0.3 mg/kg subcutaneously (SC) on the day of the procedure. In 12/18 cats, the injection was given in association with general anaesthesia or sedation. Fourteen cats survived to hospital discharge. Of 187 survey respondees, 89% routinely administered NSAIDs for surgery‐related analgesia, with 98% prescribing meloxicam and 84% of these giving it SC. Ninety percent of respondees routinely administered NSAIDs for non‐surgical‐related analgesia, with 99% prescribing meloxicam and 35% of those giving it SC. Conclusions and Relevance: We strongly recommend that practitioners avoid prescribing meloxicam SC in cats. This recommendation is emphatic in situations where concurrent dehydration and/or hypotension are possible. [ABSTRACT FROM AUTHOR]

Case report This case report describes the clinical signs and case management of a 1‐year‐old neutered male Siberian Husky that accidentally ingested 635 mg/kg of oral acetazolamide (a carbonic anhydrase inhibitor). The dog presented with severe tachypnoea due to the development of hyperchloraemic metabolic acidosis and associated hypokalaemia that persisted for 7 days. Clinical and biochemical changes resolved with intravenous and subsequent oral supplementation of sodium bicarbonate and potassium. Complete recovery occurred within 9 days of presentation. Conclusion: To the authors' knowledge, this is the first case that reports overdosage of an oral carbonic anhydrase inhibitor in a dog and subsequent recovery with adequate supplementation and supportive care. [ABSTRACT FROM AUTHOR]

This report describes the diagnosis and treatment of 16 confirmed cases of snakebite from the Australian eastern brown snake ( Pseudonaja textilis ) in dogs and cats. The clinical signs, brown snake venom antigen concentrations, coagulation parameters, and treatment outcomes following administration of an experimental caprylic acid fractionated bivalent whole IgG antivenom are documented. A brown snake venom antigen specific sandwich ELISA was used to retrospectively quantify venom levels in serum and urine. The characteristic clinical signs of envenomation in all cases were neurotoxicity to a variable extent and coagulation disturbances. The median serum venom concentration at presentation was 122 ng/mL and ranged from 1.9 to 3607 ng/mL. The median urine venom concentration at presentation was 55 ng/mL and ranged from 3.3 to 2604 ng/mL. Mechanical ventilation was used to successfully support respiration in three severely paralysed cases for 1–30 h. In four cases where serum samples were available post-antivenom treatment, venom was no longer detectable. Coagulation parameters measured on citrated plasma samples collected prior to antivenom from each case were abnormally prolonged to variable degrees in all cases. Three cases (2 dogs; 1 cat) were euthanized within four hours of presentation for either cost based reasons (2) or poor prognosis (1). One dog developed massive and potentially fatal pulmonary haemorrhage and was euthanazed. In vitro testing of the venom procoagulant neutralising efficacy of the experimental antivenom demonstrated it was 9.6–72 times more effective when compared to two other commercial veterinary antivenom products. This is the first detailed report of a case series of P. textilis envenomation in dogs and cats. The envenomation syndrome in dogs and cats differed to that reported humans, dominated by neurotoxicity and coagulopathy; unlike in humans, where coagulopathy is of primary clinical significance. [ABSTRACT FROM AUTHOR]

This study examined the usage of powered seating functions, including tilt-in-space, backrest recline, and seat elevation, among a group of wheelchair users during their typical daily activities. Twelve individuals who used a power wheelchair with seating functions participated in the study. They drove their own wheelchair and used the seating functions as needed in their community environment for about 2 weeks while the seating function usage was recorded with a portable device. We found that subjects occupied their wheelchair for 11.8 +/DS 3.4 hours a day (all data shown as mean +/DS standard deviation). While occupying their wheelchairs, they accessed tilt-in-space, backrest recline, and seat elevation 19 +/DS 14 times a day for 64.1% +/DS 36.8%, 12 +/DS 8 times for 76.0% +/DS 29.8%, and 4 +/DS 4 times for 22.5% +/DS 34.9%, respectively. Subjects chose to stay in tilted and reclined positions in their wheelchair for 39.3% +/DS 36.5% of their time each day. They spent little time in a fully upright position. Subjects changed their seating positions every 53.6 +/DS 47.0 minutes. Time spent in positions of different seating pressures varied among subjects. The information collected could enhance clinical practice of wheelchair provision, resulting in better compliance with clinical instructions and appropriate use of seating functions among wheelchair users. [ABSTRACT FROM AUTHOR]

This case report describes a dog envenomed by a red-bellied black snake (RBBS; Pseudechis porphriacus ) that experienced severe and life-threatening haemolysis. The dog presented with hypersalivation, facial swelling, mildly prolonged activated clotting time and the absence of neurological deficits. Envenomation was confirmed by positive identification of the snake and retrospective measurement of RBBS specific venom antigen (24 ng/mL) in serum. The dog was initially hospitalised, treated with intravenous fluids and one vial of tiger-brown snake antivenom which is recommended for RBBS envenomation in Australia. However, after 3.5 d the dog's PCV had declined to 15% and the dog was dull and tachycardic. A second vial of tiger-brown antivenom followed by a packed red blood cell transfusion was administered. A rapid clinical improvement within 12 h was observed. No free RBBS venom was detected in serum at any time point after the first vial of antivenom. Longitudinal haematology and biochemical profiling was performed to 62 d post-envenomation and revealed a gradual recovery in the haematocrit to normal reference range. Spherocyte numbers on blood smear were highest at 5 d post-envenomation and gradually declined to undetectable after 62 d. This case highlights the potential for unpredictable, severe and life-threatening anaemia resulting from RBBS envenomation in dogs. [ABSTRACT FROM AUTHOR]