This 2020 Small Animal medicine case was run by Jane Eastwood. Click here to follow it.
Jane also provided some further insight after the case finished:
Well done for working through some questions to help you clarify the presentation for this case and why this is important. Initial history & phys exam suggest dietary sensitivity is likely ie any adverse reaction to food. Parasites less likely (he is not a juvenile) but giardia is always possible. When thinking about differentials try to have some examples for some of the categories you come up with – for example bacterial gastroenteritis (eg salmonella, campylobacter). We were generally happy that Benji was “well” albeit with a problem (diarrhoea). Our approach would be different if he seemed unwell with a longer problem list- for example painful, dehydrated, pyrexic, vomiting. Dietary management but no other treatment was indicated at this stage- Treating any self limiting disease with a drug can easily be misinterpreted as a response to treatment. Diet advice was to give small, frequent low fat (promotes stomach emptying), bland and easy to digest meals. Rice/pasta and lean meat or eggs. We should feed diet until diarrhoea resolves and then gradually reintroduce normal food. Not suitable for a long term (weeks to months) diet. It would not be wrong to treat for giardia at this stage just to try to rule this out. Other suggestions such as probiotics are quite reasonable but perhaps not essential.
If everything goes well, a follow up appointment might be considered a “waste of money” by Benji’s owner. But we should see Benji if something changes- for example he goes off his food or seems unwell or the diarrhoea persists or changes or he is vomiting. We would usually expect his stools to be much improved within 5-10 days (often much sooner) for a simple gastroenteritis. So…we don’t need to see all cases like this back but we do need to make the owners aware of their responsibility to come back if in any doubt.
When Benji came back, I agree we might want to clarify if he seemed to be polydipsic as well as polyuric. He could just be polydipsic to compensate for water loss in diarrhoea.
It’s easy to forget the problem list but creating a problem list of primary and secondary problems helps especially with more chronic or complicated cases. Each primary problem can be used to draw up differentials (so we don’t miss anything) and then you can look for areas of overlap to help us focus on what’s most likely for our individual patient. Try to put the most useful problem (or the “diagnostic hook”) at the top of your lists. For example lethargy can be a problem but not always a useful one if there is something more useful to work with. I would always put ascites or diarrhoea higher up the list than lethargy in a case like a Benji. Prioritising is an important skill to demonstrate to show you can “see the wood for the trees”.
When discussing diagnostic tests try to be really correct in terms of what you think you can rule in or out as opposed to which tests help you look for supporting evidence in favour (or against) one of your differentials. Just as an example- can we really “rule out” hypoadrenocorticism based on haematology and biochemistry only? We might pick up markers for this disease but normal bloods won’t necessarily rule it out completely…perhaps they would just make it less likely.
We worked through the blood tests well. When ruling out renal disease a lot of people based this on absence of azotaemia and concentrated urine. Those would be important when we are thinking of “typical” CKD but remember the other group of much less common kidney diseases affecting the glomerulus where proteinuria can lead to hypoalbuminaemia and nephrotic syndrome but ability to concentrate urine and excrete products such as urea and creatinine are maintained sometimes for a long time before the disease progresses from the glomeruli. We ruled out significant renal glomerular disease in Benji with negative urine protein dipstick. If there had been some proteinuria we would have asked for a urine: protein creatinine ratio.
When thinking about ultrasound of the small intestine we focus on wall thickness and layering. Are any changes generalised?
Even if we had done some blood tests/investigations at the first consultation, they could have been normal in this case. Initial treatment was appropriate and ideally the owners should have brought him back sooner.
Benji had endoscopic biopsies taken based on the generalised mucosal thickening and increased risks of surgery with hypoalbuminaemia (eg breakdown of intestinal biopsy sites, compromised abdominal wall healing). You would need to be careful that his ascites didn’t compromise his breathing more under GA. Histopath showed the samples were good quality (ie worth looking at!) and reported a marked inflammatory infiltrate (lymphoplasmacytic) and villus blunting. This would be consistent with PLE secondary to severe chronic canine enteropathy (IBD) and there were no changes to suggest lymphoma.
We could also consider a treatment trial in a case like this if owners weren’t keen for investigations (for a wide range of owner reasons!).
- Rule out parasites: treatment trial (fenbendazole) or faecal analysis
- Consider antibiotic treatment trial for ARD if bacterial flora deranged due to leakage of fat/lymph in to lumen +/or malabsorption. Sometimes we use metronidazole- this drug might have immunomodulatory properties.
- Fat restricted diet +/- rule out diet intolerance as cause of inflammation- single source protein or hydrolysed protein exclusion diet
- Anti inflammatory/immune suppressive treatment: prednisolone likely to be the first line treatment. Might need to consider other drugs such as cyclosporine if inadequate response to treatment
- Diuretics?- often not needed but spironolactone seems to be more effective at managing ascites than furosemide. Would consider if ascites was causing discomfort- potential to have an adverse effect on GI blood flow due to increased abdominal pressure.
- Supplement cobalamin if low- worth checking serum cobalamin in any chronic GI case
Ascites can resolve very quickly if the albumin improves in to the high teens or higher. We could weigh Benji- one of the few times when we want a diarrhoea dog to lose “weight” initially- ie we want him to lose the fluid. Polydipsia should resolve as ascites resolves. He should become polyuric when he shifts fluid from the abdomen so we might warn the owners. But polydipsia/uria are hard to interpret once dogs are on prednisolone.
We can also check PCV/TS as a cheap monitoring tool rather than running biochemistry each time.
Prognosis: can be guarded although Yorkies seem to have a very steroid responsive form of PLE.
Benji: did well on prednisolone and an exclusion diet. He had cobalamin supplementation but no diuretics. He stayed on diet long term but also had recurrent signs when he stopped prednisolone so stayed on a relatively low anti inflammatory dose.
Hooray for Benji!