No abstract

Objectives The aim of this study was to describe the clinicopathological findings, management and outcome of cats with refeeding syndrome (RS) following prolonged starvation. Methods Records from four referral hospitals were searched between May 2013 and November 2019 and retrospectively evaluated. Inclusion criteria were the presence of a risk factor for RS, such as severe weight loss or emaciation following a period of presumed starvation, hypophosphataemia or a delta phosphorous exceeding 30% reduction following refeeding, being treated on the basis of a clinical diagnosis of RS and one or more derangement of hypokalaemia, hypoglycaemia or hyperglycaemia. Results Eleven cats were identified, which had been missing for a median of 6 weeks (range 3–104 weeks). Mean ± SD percentage weight loss was 46% ± 7% (n = 8). Eight of 11 cats developed hypophosphataemia with a mean delta phosphorous of −47% ± 9%. All cats were documented to be hypokalaemic. During hospitalisation, 10/11 cats developed hyperglycaemia and 7/11 cats developed hypoglycaemia. Cardiovascular, gastrointestinal and neurological signs were common. Eight of 11 cats displayed new or progressive neurological deficits after refeeding, including mentation changes and cerebellar dysfunction. All cats became anaemic and seven cats required a blood transfusion. Eight cats survived to discharge after a mean of 14 ± 4 days of hospitalisation. Six cats developed acute kidney injury (AKI; International Renal Interest Society stage 1). The presence of AKI ( P = 0.024) was associated with non-survival and maximum bilirubin concentration was significantly higher in non-survivors ( P = 0.018). Conclusions and relevance Cats with RS in this cohort had been missing, presumed starved, for more than 3 weeks. In addition to hypophosphataemia and hypokalaemia, altered glucose homeostasis and organ damage involving the liver and kidneys were common. Cats with RS appear to have a good prognosis, but prolonged intensive care is required.

A seven-month-old male entire Bulldog presented for a three-week history of progressive lethargy, exercise intolerance, hindlimb paresis, muscle atrophy and hyperaesthesia. The dog had initially been raised on the bitch’s milk before maternal illness resulted in him transitioning onto milk replacer. He was weaned onto commercial puppy food until four months of age before being transitioned onto a homecooked diet. This diet comprised of raw meat, collected weekly from a local abattoir, homecooked cereals and vegetables. The patient was oxygen-dependent on presentation, requiring 40 per cent inspired oxygen concentration to maintain normoxaemia. Investigations revealed marked osteopenia with concurrent severe hypovitaminosis D, hypocalcaemia and hyperparathyroidism; hypovitaminosis A; hypothyroidism and concurrent severe pneumonia. Despite intensive medical care, nutritional interventions and escalating oxygen therapy, the dog was euthanased due to a deterioration in respiratory function. This case report highlights the severe clinical complications associated with the consumption of a nutritionally incomplete diet.

No abstract

Objective: To report the prevalence of arterial hypertension in a population of dogs with nonassociative immune-mediated hemolytic anemia (IMHA) on presentation and during hospitalization. To determine the relationships of systolic blood pressure (SBP) with mortality and a prognostic indicator, the canine hemolytic anemia objective score.