PUPD – How not to get caught short!

Presenter – Professor Ian Ramsey BVSc Phd DSAM FHEA MRVCS DipECVIM-CA, from The University of Glasgow’s Small Animal Hospital.

After attending Professor Ramsey’s webinar on diabetes, I was keen to see him apply the same logical and case orientated approach to PUPD, and once again, I was not disappointed.

Professor Ramsey started the webinar by stating that we have a fairly restricted list of differential diagnoses for PUPD compared with other clinical signs such as vomiting and diarrhoea. This should make diagnosis of the underlying cause for PUPD relatively straightforward as long as we follow a well thought through and logical pathway. This statement concerned me a little because although I do quite enjoy working up PUPD cases, I can sometimes find them incredibly frustrating to diagnose. Professor Ramsey highlighted these concerns by stating these cases don’t always follow the rule book but by using the knowledge we have we will get there in the end.

Take ‘Kas’, an eight year old male boxer. He had a two month history of PUPD and, as is often the case, Kas’s owners have limited finances. Professor Ramsey wanted to ascertain as much information with as few tests as possible and his suggestion for a minimum database included a urine dipstick and specific gravity (SG) in combination with a biochemistry profile including urea, creatinine, glucose and calcium.

Kas’s SG was 1.014 making his urine normal, but this does not exclude PUPD as a clinical sign – only hypersthenuric urine (an SG greater than 1.035) can do this. Kas’s biochemistry results were all within normal limits except for slightly elevated liver enzymes which Professor Ramsey views as one of the least useful tests to perform when trying to diagnose PUPD. Liver enzymes will become elevated in a number of diseases including liver disease, Cushings, Diabetes Mellitus, renal disease and neoplasia, so in short, if the liver enzymes are elevated, so what.

Professor Ramsey’s next logical step in diagnosing Kas’s PUPD was to try to exclude Cushing’s disease as an underlying cause. At this stage Professor Ramsey asked the audience for their input on what test should be performed next. 71% (I fell into this category) said an ACTH stimulation test, 17% said a low dose dexamethasone test and 12% said a urine cortisol:creatinine ratio.

The clue was in the question ‘how to EXCLUDE Cushing’s disease’ making a low dose dexamethasone test the correct answer. An ACTH stimulation test will only pick up 80% of suspected Cushing’s cases whereas the low dose dex test will pick up 95% of these cases. Professor Ramsey was keen to stress that an ACTH stimulation test is appropriate as a first line test if you are confident that the clinical signs correlate with Cushing’s disease. With Kas, apart from the PUPD, he had no other signs which correlated with Cushing’s disease and in his case the ACTH stimulation test was negative but the low dose dexamethasone test was positive.

Kas was diagnosed with Cushing’s disease and a simple abdominal x-ray showed a calcified area in the region of the adrenal gland. An adrenal gland tumour was confirmed with an ultrasound scan. The case of ‘Kas’ showed us that diagnosing PUPD is not always straight forward but with a good understanding of the tests we perform, how they work and their pitfalls, we will eventually come to the right diagnosis no matter how long it can sometimes take.

The Stethoscope (MRCVS)

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