Inflammatory Pancreatic Disease
The pancreas is a unique organ possessing both exocrine (digestive) and endocrine (hormonal) functions. Inflammatory pancreatic disease affecting only the exocrine portion is extremely uncommon in young dogs and cats (). Consequently, inflammatory pancreatic disease, that is, acute pancreatitis or relapsing pancreatitis that more commonly affects older dogs and cats, has been rarely identified in dogs and cats younger than 6 months of age. The likely causes of inflammatory pancreatic disease in the young dog and cat are abdominal trauma and infectious agents. Abdominal trauma may induce pancreatitis in dogs that are traumatized by motor vehicles and in cats that have fallen or jumped from high places (high-rise syndrome) (). In addition, abdominal surgery may result in acute pancreatitis due to traumatic injury to the pancreas (spearing the pancreas with a surgical instrument) or excessive manipulation of die pancreas.
Infectious agents can occasionally contribute to inflammatory pancreatic disease. Pancreatic necrosis can be found on postmortem examination of an occasional dog afflicted with canine parvovirus infection (). It is not known whether the canine parvovirus is directly cytotoxic to the pancreatic tissue or pancreatitis occurs secondary to the invasion of enzymes and bacteria of the intestinal tract into the pancreas. In cats, pancreatitis may be associated with the effusive form of FIP (). Other infectious agents directly associated with inflammatory pancreatic disease in the young dog and cat would be extremely unusual and most likely a one-time occurrence.
Although seldom required, laboratory confirmation of inflammatory pancreatic disease includes a complete blood count, serum chemistry profile, serum amylase and lipase determinations, serum trypsin-like immunoreactivity (TLI) assay, and survey radiographs and/or ul-trasonography of the abdomen. Normal values for serum amylase and lipase activities in dogs and cats younger than 6 months of age are generally indicative of normal adult values. Hyperamylasemia and hyperlipasemia combined with typical clinical features of inflammatory pancreatic disease, as seen in adult animals, establish the diagnosis of inflammatory pancreatic disease until proved otherwise. The serum TLI assay may be increased — TLI values of more than 35 µg/L in young dogs and more than 50 µg/L in young cats are consistent with pancreatitis. Its treatment is entirely supportive and is managed in a manner similar to that for the afflicted older dog or cat.
Congenital Pancreatic Hypoplasia
By far the most common cause of noninflammatory pancreatic disease in the young dog is congenital pancreatic hypoplasia (). This disorder of young dogs is characterized by generalized reduction in pancreatic exocrine (acinar) cells, but the islets of Langerhans remain intact (). The disorder is more common in large breeds of dogs, that is, German shepherd (Alsatian), Doberman pinscher, Irish setter, Labrador retriever, and Saint Bernard, but has also been seen in the beagle (). There may be a sex predilection favoring females (), and young dogs that are symptomatic generally present before 1 year of age. Congenital pancreatic hypoplasia has not been recognized in the young cat.
Most dogs affected with congenital pancreatic hypoplasia present with signs of weight loss or failure to gain adequate weight and poor physical appearance (i.e., dull, dry haircoat and excessive shedding) despite exhibiting a good to voracious appetite. Varying degrees of frequent (6 to 10 stools per day), foul-smelling, bulky, greasy, loose stools are described by the dog owner. Often, coprophagia is noted. Affected dogs commonly eat their stools because of their high fat content and because of a dietary energy deficit. The diarrheic stools contain undigested sugars and fats that are being altered by intestinal bacteria to become osmotically active particles (). The marked increase in osmotically active particles and the subsequent efflux of water into the lumen of the intestinal tract result in the colon’s inability to resorb the increased volume, and diarrhea ensues. The volume of unabsorbed intraluminal water produces marked intestinal dis-tention and altered motility, which may be severe enough to cause intestinal and colonic bacterial overgrowth (). Unabsorbed fatty acids may also impair the absorptive capacity of the small intestine by damaging the brush border, blunting the villi, and inhibiting colonic water absorption.
The diagnostic evaluation of dogs suspected to have congenital pancreatic hypoplasia differentiates this disorder from intestinal mucosal malabsorption. Diagnosis of congenital pancreatic hypoplasia is usually not difficult because the presenting signs are rather characteristic and the laboratory test results are helpful in its diagnosis. The serum TLI assay values are classically decreased — TLI values are consistently less than 2.5 µg/L in affected dogs. When the diagnosis is still in question or serum TLI assay results are not available, an exploratory laparotomy can be used for confirmation.
Treatment of dogs with congenital pancreatic hypoplasia depends mainly on dietary management and supplementation with pancreatic digestive enzymes (). Efforts to treat these dogs are usually rewarded with a favorable response. The expense of treatment and an unconscientious owner, rather than the ineffectiveness of the treatment regimen itself, are most often the reasons that successful treatment is not accomplished. The most effective dietary management for dogs with congenital pancreatic hypoplasia is a highly digestible, low-fiber, moderate-fat diet supplemented with pancreatic enzymes (). Commercial diets formulated for gastrointestinal disease may be fed. The dog’s daily food intake is divided into two or three feedings or is fed free choice. The dietary replacement of pancreatic digestive enzymes is given orally with each meal. Various pancreatic enzyme products are commercially available for this purpose (). Reliable commercial products are available in both powder and tablet form. The usual effective dosage of the powder preparation is 1 to 2 tsp per meal for each 20 kg body weight. The pancreatic enzyme product is mixed with the commercially prepared canned or well-moistened dry dog food and fed without necessarily any preincubation time. When diarrhea is in remission and the animal is gaining weight, the pancreatic enzyme product should be titrated to the minimum effective maintenance dose per feeding.
When pancreatic digestive enzymes are given orally, a high percentage of them are inactivated by gastric acid. Even though only a fraction of the pancreatic enzymes administered reach the small intestine in an active state, they are still effective because only a slight increase in duodenal digestive enzyme activity is needed to achieve marked improvement in nutrient assimilation (). In some dogs, antimicrobial agents may be a helpful adjunctive therapy for the bacterial overgrowth of the small intestine that often accompanies malassimilation in congenital pancreatic hypoplasia (). Medium-chain triglycerides may be added to the dog’s diet if additional dietary energy is needed to increase weight gain or maintain condition in the dog that fails to respond otherwise. The medium-chain triglycerides can be used to provide up to 25% of the dog’s caloric need and, when fully utilized, provide 8 kcal/ml ().
The dog’s body weight, general condition, and stool character should be monitored weekly during the treatment of congenital pancreatic hypoplasia. Stool volume should decrease precipitously, and gains in body weight should begin soon after initiation of dietary management and the supplementation of pancreatic digestive enzymes (). The dietary replacement of pancreatic digestive enzymes is generally required for the rest of the dog’s life.
Selections from the book: “Veterinary pediatrics: dogs and cats from birth to six months”. Johnny D. Hoskins. (2001)
