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BackgroundFew studies show the detrimental effect of canine obesity on cardiopulmonary function (CPF). The 6‐Minute Walk Test (6MWT) is a noninvasive exercise test easy to perform in clinical settings.ObjectiveThe aim of this study was to investigate the effect of obesity and body weight loss (BWL) on CPF assessed by the 6MWT and arterial blood gas analysis.AnimalsSix experimental Beagles and 9 privately owned obese dogs were enrolled in a diet‐induced BWL program.MethodsArterial blood gas analysis and 6MWT were repeated in obese subjects (BCS 8‐9/9), in the middle of BWL (overweight, BCS 6‐7/9), and in lean dogs (BCS 5/9). Heart rate (HRp) and oxygen saturation (SpO2) were measured by pulse oximetry before the 6MWT, at midtest, and during a 5‐minute recovery period.ResultsTwelve dogs completed the BWL program (initial BW, 27.3 ± 2.9 kg; final BW, 20.85 ± 2.9, lsmeans ± SE, P ≤ .001). BWL caused a significant increase in 6MWT walked distance (WD; obese: 509 ± 35 m; overweight: 575 ± 36 m; lean: 589 ± 36 m; P ≤ .05). Resting arterial blood gas results were not influenced by BWL. Including all time points, obese dogs showed higher HRp and lower SpO2 compared to overweight and lean dogs. SpO2 at the end of the walk was significantly lower in obese dogs.Conclusion and Clinical ImportanceObesity negatively affects 6MWT performances in dogs. The 6MWT may be used to demonstrate the efficacy of BWL to improve CPF and quality of life in obese dogs. Although BWL induced significant improvement of cardiopulmonary parameters before ideal BW, WD improved until the end of the BWL program.

Pseudolymphoma is a drug reaction to anti‐epileptics that is well recognized in humans; it has been reported in one cat but not dogs. In this report, lymphoma‐like clinical signs are suspected to be secondary to phenobarbital administration in a dog. A 2.5‐year‐old male, neutered Shepherd mix presented for a 3‐day history of progressive ataxia, dazed mentation, pyrexia, and lethargy. While hospitalized, the dog developed generalized lymphadenopathy and sustained pyrexia. The dog was receiving levetiracetam and phenobarbital for epilepsy, and serum concentrations of both were within standard therapeutic ranges. Abdominal ultrasound revealed hepatomegaly, splenomegaly, and generalized lymphadenopathy. Cytology of the peripheral lymph nodes was consistent with reactive lymph nodes, and aspirates of the liver and spleen revealed histiocytic‐neutrophilic inflammation. Phenobarbital was discontinued and replaced with zonisamide. Within 24 hours, the dog was normothermic, and other clinical signs resolved within a week. This case highlights a potentially serious yet reversible adverse reaction to phenobarbital in a dog. This idiosyncratic reaction could be mistaken for neoplasia and is an important differential for lymphoma‐like signs in any dog administered phenobarbital.

A 9-year-old, intact male, Brie’s shepherd dog, with a 10-day history of depression and tachypnoea developed signs of central neurological dysfunction. 16 Multislice Computed Tomography (CT) pre- and postcontrast studies of the brain revealed a single intra-axial homogeneous well-circumscribed hyperattenuating (+/− 62 HU) and noncontrast-enhancing area, 5 mm in diameter, in the caudal part of the mesencephalon. This finding was highly suggestive of a haemorrhagic event. A pituitary-dependent hyperadrenocorticism (PDH) was identified and is considered likely to be the underlying cause. A repeat CT scan examination, 2 months later, showed almost complete resolution of the brain lesion. The present case describes a solitary 5 mm diameter lesion: the result of intracranial haemorrhage in a dog with presumed PDH.