Exocrine Pancreatic Insufficiency in Small Animals
Exocrine pancreatic insufficiency (EPI) is a syndrome caused by insufficient synthesis and secretion of digestive enzymes by the exocrine portion of the pancreas. EPI is less common than pancreatitis in both dogs and cats, but it is the second most common exocrine pancreatic disorder in both species.
Pancreatic acinar atrophy is the most common cause of EPI in German Shepherds, Rough Collies, and Eurasians, whereas chronic pancreatitis is the most common cause in dogs of other breeds and cats. Less common causes of EPI in dogs and cats are pancreatic or extrapancreatic masses that lead to obstruction of the pancreatic duct. The exocrine pancreas has a remarkable functional reserve, ~90% of which must be lost before clinical signs of EPI develop. Pancreatic acinar enzymes play an integral role in the assimilation of all major macronutrients, and a lack of pancreatic digestive enzymes leads primarily to maldigestion. However, animals with EPI also show evidence of malabsorption, the pathogenetic basis of which is less well understood (also see Malabsorption Syndromes in Small Animals). The nutrients remaining in the intestinal lumen lead to loose, voluminous feces and steatorrhea. The lack of nutrients also causes weight loss and may lead to vitamin deficiencies. In animals with EPI caused by chronic pancreatitis, destruction of pancreatic tissue may not be limited to the acinar cells, and concurrent diabetes mellitus may develop.
EPI due to pancreatic acinar atrophy is most frequent in young adult German Shepherds but has also been described in Rough Collies and Eurasians. Dogs and cats with EPI due to other causes are usually middle-aged to older and can be of any breed. Clinical signs most commonly reported are polyphagia, weight loss, and diarrhea. Vomiting and anorexia are observed in some animals and may be a sign of concurrent conditions rather than EPI. The feces are most commonly pale, loose, and voluminous and may be malodorous. In rare cases, watery diarrhea may be seen. In a small portion of cats with EPI, the high fat content of the feces can lead to a greasy appearance of the hair coat, especially in the perianal and tail region.
A serum trypsin-like immunoreactivity (TLI) concentration of ≤2.5 mcg/L in dogs or ≤8.0 mcg/L in cats is diagnostic for EPI. Because digestion of a macronutrient can often be accomplished by more than one enzyme, lack of exocrine pancreatic secretions does not necessarily lead to clinical signs. For example, several German Shepherds with subclinical EPI have been reported. These dogs had severely decreased serum TLI concentrations and a lack of exocrine pancreatic tissue, but no or only intermittent clinical signs of EPI.
An assay that measures fecal elastase in dogs has been validated. Unfortunately, some healthy dogs or dogs with chronic small-intestinal disease may have a severely decreased fecal elastase concentration, making this test much less reliable than serum TLI concentration.
Most dogs and cats with EPI can be successfully treated by supplementation with pancreatic enzymes. Powder is more effective than tablets, capsules, and especially enteric-coated products. Initially, 1 teaspoon/10 kg should be given with each meal for dogs and 1 teaspoon/cat with each meal for cats. Once the clinical signs have completely resolved, the dose can be slowly decreased until the lowest effective dose has been reached. However, it should be noted that the lowest effective dose can vary between enzyme batches. Oral bleeding has been reported in 3 of 25 dogs with EPI treated with pancreatic enzyme supplements; the bleeding stopped in all three dogs after a dose reduction. Moistening the food and pancreatic powder mix may also decrease the frequency of this adverse effect.
Fresh pancreas may be a viable alternative to the use of powder; 1–3 oz (30–90 g) of raw chopped pancreas can replace 1 teaspoon of pancreatic extract. Raw pancreas can be kept frozen for several months without loss of enzymatic activity. Preincubation of the food with pancreatic enzymes or supplementation with bile salts is not necessary.
Even though pancreatic enzyme supplementation decreases the clinical signs in almost all animals, nutrient absorption, especially that of fats, is not normalized. Feeding low-fat diets to accommodate impaired fat digestion has been suggested, but this may further decrease fat assimilation and lead to deficiencies of fat-soluble vitamins and/or essential fatty acids. Some types of dietary fiber interfere with pancreatic enzyme activity, and a diet low in insoluble or nonfermentable fiber should be fed.
Enzyme supplementation alone may not lead to complete resolution of clinical signs; cobalamin deficiency should be considered as a possible cause. Cobalamin absorption depends on adequate synthesis and secretion of intrinsic factor. In both dogs and cats, the majority of intrinsic factor is synthesized and secreted by the exocrine pancreas, and >80% of dogs and almost all cats with EPI are cobalamin deficient. Also, cobalamin deficiency was the only independent risk factor for poor outcome in a study of dogs with EPI. Thus, serum cobalamin and folate concentrations should be routinely evaluated in small animals with suspected EPI. Dogs and cats with cobalamin deficiency, suggested by a severely decreased serum cobalamin concentration, should be parenterally supplemented with cobalamin. Other hypovitaminoses have also been reported in animals with EPI. For example, vitamin K deficiency leading to a coagulopathy has been reported in some cats with EPI.
Some animals may not respond to enzyme supplementation and cobalamin therapy and likely have concurrent small-intestinal disease. Animals with EPI commonly have concurrent small-intestinal dysbiosis and may need antibiotic therapy. Inflammatory bowel disease also occurs in some animals with EPI. In those that do not respond to therapy, a proton pump inhibitor can also be tried.