Introduction: Hyperbilirubinaemia is an important clinicopathological finding in canine medicine. The objectives of this study were to describe the clinical presentation and outcome of dogs with hyperbilirubinaemia; also to identify factors associated with survival. Materials and methods:Retrospective study of dogs with hyperbilirubinaemia from two referral centres in South Australia (2015)(2016)(2017)(2018)(2019)(2020). Signalment, clinical signs, clinicopathological data, diagnosis and outcome were obtained from searching clinical records. Univariable analysis and logistic regression modelling were used to compare outcomes and overall survival. Results: A total of 115 cases were included. The most common clinical signs were vomiting (63.5%), anorexia (62.6%), lethargy (55.7%) and pyrexia (18.3%). Pre-hepatic icterus was diagnosed in 18 cases (15.7%), hepatic icterus in 51 cases (44.3%) and post-hepatic icterus in 42 cases (36.5%). The median survival time across all cases was 40 days (95% confidence interval [CI]: 9-126 days). There was an increased risk of death in dogs with serum bilirubin greater than 60 μmol/L at diagnosis (odds ratio [OR] = 3.55; 95% CI: 1.53-8.22; p-value = 0.003) and in dogs with pre-hepatic icterus compared to hepatic (OR = 4.35; 95% CI: 1.18-16.0; p-value = 0.027) and post-hepatic icterus (OR = 6.52; 95% CI: 1.67-25.5; p-value = 0.007). Conclusions: Pre-hepatic icterus was associated with a significantly higher risk of death than hepatic and post-hepatic icterus. Serum bilirubin >60 μmol/L at diagnosis was associated with a significantly shorter median survival time. This cut-off may be useful in discussions with owners regarding pursuing further diagnostic investigation and treatment. Further prospective studies are needed to prove the validity of this cut-off.
Case summary An 8-month-old female spayed Burmese cat was referred for investigation of reduced appetite, reluctance to walk and jump and amaurosis. On serum biochemistry there was severe hypokalaemia and marked elevation of creatine kinase, suggestive of hypokalaemic polymyopathy. The neurological signs were consistent with thiamine deficiency. The cat was negative for the periodic hypokalaemic polymyopathy (PHP) of Burmese cats, and was ultimately diagnosed with a previously undescribed potassium wasting nephropathy requiring ongoing oral potassium supplementation. The response to treatment was excellent and the cat has remained clinically normal over a 12-month follow-up period. Relevance and novel information PHP in Burmese cats has been well described, but all cases to date have been shown to be secondary to a genetic mutation in WNK4, resulting in potassium wasting into the urine. This is the first case report of another potassium wasting nephropathy in a young Burmese cat, with subsequent development of nutritional thiamine deficiency.
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