PERRY is a dog with diarrhoea. You’ve seen his owners on-and-off in the waiting room, visiting your colleagues for annual health checks and the odd digestive upset which you see on his history.
A normally very active twoand-a-half-yearold German Shepherd, you can’t help but let your mind jump into pattern recognition mode as he enters the consultation room. That’s no excuse not to be systematic in your approach of course; this is a repeat occurrence, but with a recent drop in Body Condition Score from 4/9 to 3/9 things are getting serious.
Previous episodes have been managed as acute upsets, with low-fat dietary management (this food has never been purchased from the practice in the long-term), metronidazole or oxytetracyclines, fenbendazole anthelmintics and at least one course of steroids slipping through the net.
This approach has managed signs on at least three occasions thus far but the introduction of these empirical treatments hasn’t been orderly, often with many modes of intervention being staged simultaneously.
You question Perry’s guardians further while keeping a close eye on his behaviour in the consulting room. He is alert but his disinterest is obvious; certainly not what you’d expect from a young, normally boisterous Shepherd.
On the mention of “diarrhoea” you immediately go into classification mode. Quick-fire questions establish that we’re dealing with relatively large volumes (with at least six visits to the garden throughout the day) of poorly formed stools varying in colour from brown to yellow which are agreed to be “greasy” upon your candid descriptions and showing some (unpleasant) images.
No strangers to managing these deposits in the park, Perry’s owners have taken a pro-active approach in finding a diet which produces the bestquality stools possible.
Apart from trying the expensive low-fat veterinary formulas, they’ve explored three other foods over the last 12 months and settled on a natural food with named chicken and oat ingredients which (thanks to a quick Google search) you note is labelled “higher in natural fibre”.
Justifiably, your owners are now questioning whether this is the correct food for him to stay on in the longterm.
Another key point you pick up in your extended history is the concern over weight loss. They’ve seen a loss of 1-1.5kg over the last fortnight and at just over 30kg, Perry has never been a particularly heavy dog, regardless of the fact that he enjoys his food.
Recently he never fails to ask for another bowl as soon as he’s finished his first, almost to the point of what sounds like aggressive food-guarding from the owner’s descriptions.
Unrewarding examination
Physical examination isn’t massively rewarding in this case. You find vital signs within normal limits, that Perry is 5-10% dehydrated, his skin is dry and coat quality poor with dander and three or four localised patches of thinning
hair. Moving to the abdomen you auscultate increased gut sounds and are careful to feel slightly dilated and thickened intestinal loops.
A rectal examination yields no pain, mucosal abnormalities, mucus or blood. The most remarkable change is the aforementioned loss of “bounce” you’d expect from a dog of this age as well as his worrying weight loss.
Given that the current bout of diarrhoea has occurred over the last two weeks and that the loss of condition you’re seeing marks the seriousness of Perry’s condition, you’re pleased to hear that your concerned owners are on-side when it comes to collecting a GI database.
We always should work with the samples nature gives us of course and in this case, a faecal sample isn’t difficult to come by. After a 20-minute walk what returns to your lab is indeed foul-smelling, poorly formed and yellow/ochre in colour.
You surge forth with your investigation and indeed, find a mild anaemia on haematology and low cobalamin, reducing your differential list even further.
You’re not surprised when trypsinlike immunoreactivity (TLI) indicates quite plainly an exocrine pancreatic insufficiency (EPI).
The exocrine pancreas has wideranging roles. We all know it to secrete lipase, trypsin and amylase enzymes, responsible for digesting fats, proteins and carbohydrates respectively.
Beyond the acinar cells, however, the duct cells secrete bicarbonate; central to keeping pH in check and allowing the entire digestive and absorptive process to occur as it should. Intrinsic factor allows the absorption of cobalamin and peptides/defensins regulate the upper GI flora.8
Given all of these key roles in digestion go amiss in EPI it’s no wonder the patient swiftly moves into protein-calorie malnutrition.
We’ve an obvious case of malassimilation here. Nutrients sufficient to maintain body condition are quite simply not able to pass across the intestinal barrier at a fast enough rate.
Apart from the body’s lean muscle mass having a high metabolic demand, the skin and coat is responsible for much of the draw on dietary protein. It suffers greatly in this malabsorptive state.
Compounding the matter for Perry is the selection of a high-fibre food. While his owners have the best intentions in relieving Perry of his poor stool quality, the discomfort and mess this brings, you recall that fibre (particularly when insoluble) can not only regulate faecal quality but retard the absorption of other nutrients.
Much to your chagrin you look again at the food that’s currently being fed and note that weight control is among its many suggested uses. In the face of an insatiable appetite, now known to be driven by poor digestion, the owners haven’t picked this up as a potential problem, until you look at the product’s caloric content together.
Dietary problems here are therefore three-fold:
- The defective exocrine function of Perry’s pancreas reduces the nutrients available for intestinal absorption.
- An increased fibre load modifies the composition and transit of ingesta through the lumen, interfering with the absorptive process particularly when insoluble fibres are high.
- Fibre, with a low caloric content, dilutes calories, meaning that Perry’s overall energy requirements will be more difficult to fulfil.
All things considered, Perry is indeed in a dangerous place from a nutritional standpoint.
The historical approach to feeding the EPI case is to select for diet digestibility, relatively low fibre and low-to-moderate fat level.4 Firstly we want to be sure that most of what’s entering the GI tract isn’t coming out the other end.
In the EPI patient, a low level of nutrient digestion means increased susceptibility to antibiotic responsive diarrhoea (sometimes referred to as small intestinal bacterial overgrowth) where unabsorbed protein and carbohydrate passes through the small intestine to feed an atypical bacterial load.
Gaseous bacterial fermentation products and fluid are drawn into the lumen by an osmotic gradient and lead to many GI symptoms – borborygmi, flatulence and putrid stools being the most offensive.
Low fibre rations are indicated for the above reasons; to counter any impedance this may bring to the absorptive process and to make way for highly digestible, more energy- and nutrient-rich fractions to complete the formula. Low caloric density is certainly not a priority in EPI cases.
In relation to fat, however, thoughts over the last 10 to 15 years have evolved. Fat is considered the most difficult nutrient to assimilate and lipase activity is the limiting step in digestion.7 Where greasy steatorrhoea is seen, the temptation is to jump to the conclusion that fat should be restricted as much as possible.
Studies putting this assumption to the test have given varied results: borborygmi, flatulence and faecal volume were reduced in eight out of 14 dogs fed for four weeks 10 v. another study where diets with up to 43% calories from fat promoting better protein, fat and carbohydrate digestibility compared to those containing 18 and 27% of calories from fat.9 All considered, it seems that faecal fat output is more dependent on the digestibility of the fat rather than the total amount fed.7
Following a lengthy conversation with the nurse in the practice who is most keyed up in nutrition, you feel you have two possible dietary strategies to pursue alongside exogenous enzymes: either a hydrolysed diet or a low-residue (higher-fat) gastrointestinal formula. Both seem to have their advantages, the former with a focus on reduced allergenicity and the latter prioritising palatability and gut-tropic effects.
Given your owners’ selectingredient focus, and that all of your preferred outcomes (high tolerance, improved faecal quality, hair coat and weight-gain) were demonstrated in a three-patient case study of German Shepherds 1 , you opt for a soy hydrolysate and rice formula.
Giving instructions for a gradual transition, frequent small meals so as to avoid overwhelming digestive capacity and incorporation of a powdered enzyme supplement, you’re confident that a move away from Perry’s current diet to one which prioritises digestibility will make a marked difference to his overall condition… and bounce.
References and further reading
1. Biourge, V. and Fontaine, J. (2004) Exocrine pancreatic insufficiency and adverse reaction to food in dogs: a positive response to a highfat, soy isolate hydrolysate-based diet. Journal of Nutrition 134: 2166S-2168S.
2. De Lorenzi, D., Elliot, D., Frieche, V., McNeill, E., Rodrigez, C. and Tams, T. (2010) Veterinary Focus Special Edition: Pitfalls in GI disorders in the dog. Aimargues, Royal Canin.
3. Hall, E. (2012) Canine chronic enteropathy – antibiotics, diet or steroids? In: proceedings of the London Vet Show, London.
4. Hand, M., Zicker, S. and Novotny, B. (2011) Exocrine Pancreatic Insufficiency. In: Small Animal Clinical Nutirition Quick Consult. Kansas, Mark Morris Institute, 204-208.
5. Schaer, M. (2010) Exocrine Pancreatic Insufficiency. In: Clinical Medicine of the Dog and Cat. London, Manson Publishing, 432-436. 6. Simpson, K. (2013) Managing canine inflammatory bowel disease. Veterinary Focus 23 (2): 29-36.
7. Simpson, K. (2006) The role of nutrition in the pathogenesis and the management of exocrine pancreatic disorders. In: Pibot, P., Biourge, V. and Elliott, D. (eds). Encyclopaedia of Canine Clinical Nutrition. Paris, Aniwa, 162- 175.
8. Simpson, K. (2005) How I treat… Exocrine pancreatic insufficiency. Veterinary Focus 15 (2): 10-12.
9. Suziki, A., Minzumoto, A. and Rerknimitr, R. (1999) Effect of bacterial or porcine lipase with low- or high fat diets on nutrient absorption in pancreatic-insufficient dogs. Gastroenterology 116: 431-437.
10. Westermarck, E., Junttilla, J. and Wiberg, W. (1995) Role of low dietary fat in the treatment of dogs with exocrine pancreatic insufficiency. American Journal of Veterinary Research 56: 600-605.
