Pancreatitis in Cats: Diagnosis and Management of a Challenging Disease

Introduction

In contrast to classic acute pancreatitis in dogs, feline pancreatitis can be a very difficult disease to diagnose, and it requires a combination of clinical suspicion, appropriate physical examination findings, elevations in serum feline pancreatic lipase immunoreactivity (fPLI) concentrations, and changes on abdominal ultrasonography consistent with pancreatic disease. Like the disease in dogs, however, treatment remains symptomatic and supportive, because a specific cause to be addressed is rarely identified. The diagnostic difficulties encountered with feline pancreatitis are in great measure related to a lack of specific and readily attributable clinical signs. For example, vomiting occurs less commonly in cats than in dogs, abdominal pain is often present but may be difficult to detect, and the most commonly reported signs are anorexia and lethargy.¹ In addition, the sensitivity and specificity of the diagnosis of pancreatitis are highest when a combination of tests (i.e., fPLI and abdominal ultrasonography) are utilized.^2,3 Even when these tests are employed, the diagnosis is still problematic in cats with chronic pancreatitis because of the waxing and waning nature of the disease, the lack of consistent ultrasonographic changes, and a reduced sensitivity of the fPLI assay from less enzyme release.^3,4

The purposes of this paper are to review the current literature on both acute and chronic pancreatitis in cats, to discuss the best available diagnostic tests for these diseases, and to provide an overview of the important aspects of treatment of pancreatitis.

Overview of the Clinical Problem

The true incidence of pancreatitis in dogs and cats is unknown. A necropsy study, reported in 1990, of over 6000 feline pancreata in Europe showed that only 1.3% of the glands had significant pathological lesions.⁵ These results inferred that pancreatitis is a relatively uncommon clinical problem; however, anecdotal clinical evidence and improvements in the ability to diagnose pancreatitis in cats suggest that the true incidence of the disease may have been greatly underestimated. It is thought that pancreatitis is increasingly common in cats in the United States, possibly from differences in dietary or environmental management. The clinical spectrum of pancreatitis in cats may include mild, subclinical disease that does not require the attention of a veterinarian; severe, necrotizing pancreatitis for which significant veterinary care is necessary for the cat’s survival; and chronic disease with signs that may wax and wane over months or years.⁶

Pancreatitis in cats is a disease characterized by the destruction of pancreatic tissue from autodigestion by activated digestive enzymes. No cause is identified in the majority of cats with pancreatitis. The disease is frequently classified as idiopathic; however, specific causes such as infections with Toxoplasma gondii, Amphimerus pseudofelineus, and other agents should be carefully considered.⁷ Known causes or risk factors for pancreatitis in dogs, such as drugs, trauma, surgical manipulation, or ischemia are likely to be important in cats, but their relationship is so far unproven. The roles of inflammatory bowel disease (IBD) and cholangiohepatitis in the development of pancreatitis (i.e., the so-called triad disease of cats) are also poorly defined.⁸ It is clear that some cats with pancreatitis, especially those with chronic pancreatitis, also have inflammatory infiltrates in their intestine (consistent with IBD) and/or in their liver, and these cats often improve with corticosteroid therapy. Thus, a thorough diagnostic evaluation of cats with suspected pancreatitis should include intestinal (and possibly liver) biopsies to determine the extent of the problem, which can significantly influence therapeutic dietary and drug selections.

In the only reported study to date of the clinical signs of feline pancreatitis, the most common clinical signs were anorexia (100%), lethargy (97%), and dehydration (92%).¹ Additional clinical signs (in decreasing order of prevalence) included hypothermia, vomiting, abdominal pain, a palpable abdominal mass, dyspnea, diarrhea, and ataxia.¹ An important and distinct difference in cats with pancreatitis when compared to dogs, was the low incidence of vomiting and abdominal pain. However, because abdominal pain may be more difficult to assess in cats, pain may be an under-reported aspect of this disease. In cats that were presented for evaluation of pancreatitis at Texas A&M University’s Feline Medicine Service, pain was a common clinical finding and was reported in at least 75% of cats with pancreatitis (i.e., confirmed by increases in canine pancreatic lipase immunoreactivity [cPLI] and ultrasonographic changes).^a Clinical signs of pancreatitis are caused by pancreatic inflammation and its local or systemic effects. It is possible that the clinical response (i.e., inconsistently painful) observed in cats reflects a different degree of local inflammation, a different systemic response, or a requirement for more deft palpation skills to elicit evidence of clinical pain. Because the clinical signs of feline pancreatitis are often nonspecific, it is important for practitioners to consider the disease in any cat with anorexia, lethargy, or vomiting of unknown cause.

Diagnosis

The clinical presentation of canine pancreatitis is often predictable, namely that of an obese dog fed a high-fat diet or a new food, or a dog that has scavenged in garbage and subsequently developed anorexia, severe vomiting, and cranial abdominal pain.⁹ In contrast, the clinical presentation of a cat with pancreatitis is anything but routine. Cats are as likely to be underweight as overweight, and high-fat diets or a sudden change in diet do not appear to be important predisposing factors.⁹ Cats of all ages, sexes, and breeds are affected; however, in a recent report, 83% of affected cats were domestic shorthairs and 54% were neutered males.¹⁰ In addition to the history and clinical presentation being variable in cats with pancreatitis, changes on routine laboratory tests are often inconclusive. In a study by Hill et al., the most common laboratory abnormalities were not specific for pancreatitis.¹ Cats with severe necrotizing pancreatitis may also be icteric or in shock, which necessitates the consideration of a severe hepatopathy or hemolytic crisis as well. Many other conditions may also develop concurrently with pancreatitis, including hepatic lipidosis, cholangiohepatitis, IBD, interstitial nephritis, diabetes mellitus, or vitamin K-responsive coagulopathy.^10–12 Thus, a careful and complete evaluation of the cat requires consideration of each of these differential diagnoses during the formulation of the diagnostic plan.

Diagnostic evaluation of cats with suspected pancreatitis should minimally include a complete blood count, serum biochemical profile, urinalysis, abdominal radiography and/or ultrasonography, and serum assays of hepatic function (e.g., bile acid assay or urine sulfated bile acids if icterus is not present), pancreatic function (i.e., fPLI), and gastrointestinal (GI) function (e.g., cobalamin, folate).^3,9,10 Thoracic radiography is indicated in cats with concurrent pulmonary or cardiovascular disease and in those cats with suspected pleural effusion secondary to pancreatitis. For outdoor cats with potential exposure to infectious agents or intermediate hosts, tests for Toxoplasma gondii (i.e., T. gondii serum immunoglobulin [Ig] IgM and IgG antibodies) and treatment of the liver fluke, Amphimerus pseudofelineus, with praziquantel are indicated.

Hematological abnormalities in cats with pancreatitis may include nonregenerative anemia (especially in chronic cases), leukocytosis (more often seen in necrotizing pancreatitis or in cats with a pancreatic abscess), or leukopenia (less common).^1,9 Serum biochemical profile changes are also usually nonspecific and may include elevations in serum alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin, cholesterol, glucose, blood urea nitrogen (BUN), or creatinine.¹ The most common electrolyte abnormalities are hypokalemia and hypocalcemia.^1,10 When hypocalcemia is present, especially when ionized calcium levels are <1.0 mmol/L (range 1.8 to 1.17 mmol/L), a poorer prognosis and more aggressive form of therapy are indicated, because this abnormality is usually found in cats with severe, acute necrotizing pancreatitis.¹⁰

Many laboratories still report lipase and amylase activities on biochemical profiles. Serum lipase may be increased early in acute pancreatitis, but in a recent study, amylase and lipase were found to be of little diagnostic value in distinguishing normal cats from those with pancreatitis.¹² Serum lipase and amylase are derived not only from the pancreas in the dog, but also from other origins. The same is true in the cat. Also, levels are affected by multiple conditions, such as IBD, azotemia, and other inflammatory diseases.¹³ Amylase is of no use in cats for the diagnosis of pancreatitis, partly because cats make very little amylase (i.e., 10% of the activity of dogs), and serum amylase levels are often low in cats with confirmed pancreatitis.^9,14,15 In the urinalysis, no consistent changes specific for pancreatitis in cats are observed.⁹

Specific tests of GI and pancreatic function (e.g., cobalamin, folate) are very useful in the diagnosis of pancreatitis and in assessing the role of concurrent GI diseases in cats.^16,17 The serum trypsin-like immunoreactivity (TLI) assay was developed initially for dogs (cTLI) and then for cats (fTLI) as the definitive test for exocrine pancreatic insufficiency (EPI).^18,19 The fTLI assay has been used more often as a diagnostic test for acute pancreatitis in cats than as a primary diagnostic test for EPI, in part because EPI is relatively rare in cats. The premise for using the fTLI assay in cases of pancreatitis is based on an elevation in serum concentrations that are consistent with pancreatic leakage or inflammation. While an increase in fTLI can be found in cats with acute pancreatitis, the sensitivity of the test has been low (33%), and the presence of a normal fTLI does not rule out pancreatitis.²⁰ One reason for a normal TLI in the presence of pancreatitis is that the leakage of many pancreatic enzymes (including TLI) decreases rapidly after the acute insult, because these enzymes are rapidly scavenged by endopeptidases (e.g., α-2 macroglobulin, α-1 proteinase inhibitor), whose role is to inactivate enzymes released from the pancreas.²¹ Therefore, if the fTLI test is not performed within the first several hours after onset of pancreatitis, the results may be equivocal or even normal.²⁰ Furthermore, in chronic or low-grade pancreatitis, the leakage of enzymes is often not great enough to be detected by this assay.^19,20 While an increase in fTLI is specific for pancreatic enzyme leakage, it is not sensitive enough to be a definitive test for pancreatitis.

To provide a more accurate test of pancreatic inflammation, an enzyme-linked immunosorbent assay (ELISA) specific for pancreatic lipase immunoreactivity (PLI) was developed by the Gastrointestinal Research Laboratory at Texas A&M University.²² The assay is species-specific and initially was available only as a canine assay. More recently, a fPLI was developed and validated, and to date it is the most reliable measurement of elevations in pancreatic lipase, a condition consistent with acute pancreatitis.⁴ In a recent study of cats with acute pancreatitis, the assay was highly sensitive and specific (80% sensitivity in severe pancreatitis, 80% specificity).³ When used in combination with abdominal ultrasonography, the assay exceeded the sensitivity of all other available tests, including fTLI, abdominal ultrasonography alone, computed tomography (CT), and magnetic resonance imaging.³ The reference range for this assay is 2 to 6 μg/L, with possible upper limits of normal extending to 12 μg/L. In one study, cats with fPLI values >12 μg/L were confirmed to have pancreatic inflammation on biopsies taken either at surgery or necropsy examination.³ Although the fPLI assay is more sensitive than the fTLI assay for cats with mild or low-grade, chronic pancreatitis (i.e., 54% sensitivity for the PLI compared to 8% for TLI), no highly sensitive test is yet available for this form of the disease.³ It is essential to utilize the combination of history, physical examination, laboratory data, and imaging modalities along with the measurement of fPLI in making a diagnosis of chronic pancreatitis in the cat.

Imaging studies are frequently used to help identify cats with acute pancreatitis; however, many changes are subjective and inconsistent. The most common radiographic abnormalities found are generalized or focal (i.e., in the upper right quadrant) loss of peritoneal detail (suggesting peritonitis or peritoneal effusion), the presence of a mass in the area of the pancreas, hepatomegaly, dilated intestinal loops, and/or a fluid-filled duodenum.²³ These findings are not specific for feline pancreatitis, however, and the sensitivity of plain radiography for diagnosing pancreatitis is very low.⁹ Ultrasonography is a very useful tool in the diagnosis of pancreatitis, if stringent criteria are applied to the examination.^2,3 For example, an enlarged pancreas alone is not sufficient to make a diagnosis of pancreatitis, as pancreatic edema is not diagnostic for pancreatic inflammation.^2,24

A variety of echogenic changes have been reported in cats with pancreatitis, including a normal pancreas, a hypoechoic pancreas from pancreatic necrosis, a hyperechoic pancreas from fibrosis or mass formation, a hyperechoic mesentery from fat necrosis, a hypoechoic region around the pancreas from edema, a mass effect (e.g., pancreatic abscess, pseudocyst formation), and changes in the biliary tract (e.g., dilated common bile duct, sludging of bile in the gallbladder, dilated pancreatic duct).²⁴ Unfortunately, the sensitivity of ultrasonography used alone is generally low (ranging from 11% to 35%).^20,24 The noninvasive diagnostic test of choice for pancreatitis in humans is CT; however, the expense, inconsistent availability, difficulties in imaging the normal feline pancreas, and the problems encountered when imaging the pancreas with air present in the duodenum all make CT less attractive and unrealistic for routine use in cats. A recent study also revealed that when abdominal ultrasonography and fPLI were used in combination, they were far superior to CT in the diagnosis of feline pancreatitis.³

The most reliable methods for making an accurate diagnosis of pancreatic disease remain direct visualization and histopathology. However, these methods are invasive, expensive, and, in many cases, potentially dangerous if the cat is hemodynamically unstable. Furthermore, in a recent study of dogs with experimentally-induced pancreatitis, pancreata were removed and sectioned every 2 cm to determine if pancreatitis was a focal or regional disease.⁹ In half of the dogs with acute pancreatitis and two-thirds of the dogs with chronic pancreatitis, evidence of pancreatic inflammation was found in <25% of the sections.⁹ These results illustrate the potentially focal nature of the disease and emphasize the fact that while histological evidence of inflammation proves pancreatitis, lack of it does not rule out pancreatitis.⁹

Treatment of Acute Pancreatitis

Severe, necrotizing acute pancreatitis in cats can be a therapeutic challenge. As with the treatment of affected dogs, the traditional therapeutic approach is supportive and aimed at restoring circulating blood volume with intravenous (IV) fluid therapy, allowing the pancreas to rest by restricting oral food and water intake, controlling vomiting, and providing pain relief. If an inciting cause can be identified, it is also addressed. In most cases of moderate pancreatitis, this approach is highly effective, and the disease has a good prognosis.

The key to survival is the early recognition of severe pancreatitis, so that more aggressive support can be properly instituted. The most important clinical indicators of severe pancreatitis in the cat are multiple abnormalities, especially hypoalbuminemia and hypocalcemia, on the biochemical profile; severe dehydration (>8% to 10%); and the presence of tachycardia, tachypnea, or pyrexia, which are indicators of systemic inflammatory response syndrome (SIRS).²¹ Treatment of these very ill cats involves aggressive fluid therapy to correct dehydration, maintain fluid volume, and prevent further pancreatic ischemia [Table 1]. Colloid support with hetastarch or plasma is also indicated and is usually highly beneficial. Both colloidal fluids and plasma promote maintenance of plasma oncotic pressure and circulating fluid volume and help to reverse the cascade of events in SIRS.²⁵ Administration of plasma is the optimal therapy, as it not only serves as a colloidal agent via replacement of albumin and other high molecular-weight proteins, but it also provides clotting factors and the proteinase inhibitors needed to scavenge the activated pancreatic enzymes.⁸ The importance of plasma in providing proteinase inhibitors and albumin is controversial, but the oncotic support it provides is well established.

If the cat is unable to tolerate water or food after a 2- to 3-day fasting period, alternative routes of nutritional support must be considered to prevent the development of hepatic lipidosis, protein/calorie malnutrition, gut atrophy, and bacterial translocation.^14,26 The preferred method of nutritional support for humans with pancreatitis is placement of a jejunostomy tube.²⁷ Alternatively, if a jejunostomy tube cannot be placed or if enteral nutritional support is unsafe in humans, total parenteral nutrition (TPN) is instituted.²⁸ When possible, enteral nutritional support is preferred over parenteral nutrition in cats with severe pancreatitis. If feasible, the nutritional support should be provided via a jejunostomy tube. Placement of a jejunostomy tube in a cat requires anesthesia and usually abdominal exploratory surgery, so it is not frequently performed.

In cats for which a jejunostomy tube is not an option, IV nutrition provided either as partial parenteral nutrition (PPN) or TPN is a viable alternative. While enteral nutrition is always preferred, parenteral nutrition can be life-saving in cats that do not tolerate enteral feeding. Total parenteral nutrition solutions are hyperosmolar and must be delivered through a central venous catheter. The logistics of stocking and compounding the required solutions and of placing and caring for central venous catheters, as well as the need for continuous monitoring, have limited the use of TPN to large practices and teaching hospitals.

In recent years, major innovations in catheters (i.e., less thrombogenic, less prone to kinking) have made use of PPN nutrition more practical and possible. While drawbacks and limitations to PPN still exist, the process has been greatly simplified. In general, PPN is used in cats requiring nutritional support for <1 week, because it is intended to fill the gap until better or more complete nutritional support can be provided. It is used to provide up to 50% of the animal’s 24-hour energy needs, so unlike TPN, PPN cannot be the only source of nutritional support for more than a few days.

Peripheral parenteral nutrition does not require a central venous line. A dedicated, peripheral IV catheter is required (i.e., fluids are administered through another catheter). Silicone elastomer or polyurethane catheters appear to be less thrombogenic than the commonly used Teflon catheters. The catheter must be inserted using an aseptic technique, because PPN solutions are ideal media for the growth of bacteria. Opening the connections to PPN catheters should be minimized, and drip sets should be changed every other day.

The basic PPN solution is a protein source (8.5% amino acid solution), a carbohydrate source (5% dextrose), and a fat source (20% lipid emulsion), with added vitamins, minerals, and electrolytes. The key difference between PPN and TPN solutions is their osmolarity. The osmolarity of a TPN solution is often >1200 mOsm/L, while the osmolarity of many PPN solutions is <800 mOsm/L. Peripheral parenteral nutrition solutions must be mixed under aseptic conditions and in a specific order. It is best to have them formulated by a pharmacist, and they must be used within 24 to 36 hours once administration is started.

Delivery of PPN solutions is done continuously via an infusion pump. Both slow initiation and slow cessation of PPN administration is essential to prevent metabolic crises (e.g., hypoglycemia, hyperglycemia, hypertriglyceridemia, etc.). The amount of calories to be administered is determined using the same calculations as for enteral nutrition [Table 2].

Volume overload can occur in cats with congestive heart failure, renal failure, and low body weights. Intravenous fluid rates must be adjusted to account for the added volume. The most serious complications of PPN are venous thrombosis and septicemia secondary to catheter infection or solution contamination.²⁹ Scrupulous attention to aseptic handling of all components and catheter care is essential. Any change in body temperature should be immediately assessed and addressed.

For cats that are not vomiting or in which vomiting has been controlled with appropriate drug therapy, and for cats that have not eaten for >3 to 4 days or have known or suspected hepatic lipidosis, placement of an esophagostomy or percutaneous endoscopic gastrostomy (PEG) tube is a good alternative. Although most dogs with pancreatitis are treated via complete gut rest (i.e., nothing per os [PO]), cats have unique nutritional requirements, and starvation for more than a few days is unacceptable. Table 3 provides some steps for planning enteral nutritional support for cats with pancreatitis. It is important to understand that cats with pancreatitis need to be fed. If the cat is not vomiting, then food is supplied despite the pancreatitis. If the cat is vomiting, then nutritional support is provided either through a jejunostomy tube, via PPN, or by TPN until the vomiting is controlled and other forms of enteral nutrition can be instituted.

Drug Therapy

In addition to fluid therapy and nutritional support, several other aspects of therapy must be considered in cats with pancreatitis, such as pain management, control of nausea and vomiting, antibiotic usage, and antithrombotic therapy.^6,30 An important aspect of supportive care for any cat with pancreatitis is pain control, even if the cat is not showing overt signs of pain. Pain relief can be achieved in some cats with intermittent drug therapy using buprenorphine^b (0.005 to 0.01 mg/kg IV or intramuscularly [IM] q 4 to 8 hours), meperidine^c (1 to 2 mg/kg IM q 2 to 4 hours), or butorphanol^d (0.2 to 0.4 mg/kg IM q 2 to 4 hours). Some cats with severe abdominal pain require constant-rate infusions (CRI) of lidocaine^e (20 μg/kg per minute IV) or ketamine^f (2 to 20 μg/kg per minute or 0.1 to 1.2 mg/kg per hour IV) used with buprenorphine or other opioid drugs.^30,31 Low-dose lidocaine CRI also provides prokinetic activity, which can be an important benefit in cats with duodenal ileus.^31,33 Morphine should be avoided, as it can cause spasm of the pancreatic duct.⁹ Anti-inflammatory therapy with nonsteroidal anti-inflammatory drugs is not recommended because of their GI and renal side effects, especially in hypovolemic animals.

Although bacteria do not play a primary role in pancreatitis, the pancreatic necrosis that occurs in many affected cats is an ideal environment for bacterial colonization. Long-term fasting may also lead to reduced villous epithelial height within the small intestine, which predisposes the cat to bacterial translocation. The true frequency of bacterial sepsis in cats with severe pancreatitis is unknown, but pancreatic abscesses and pseudocysts are frequent complications of cats with severe pancreatitis.³² The organisms most likely to colonize the severely diseased pancreas are gram-negative and anaerobic bacteria from the GI tract (e.g., Escherichia coli, Klebsiella spp., Enterobacteriaceae spp., Clostridium spp., etc.). The antibiotics chosen for cats with ultrasonographic evidence of pancreatic abcessation or systemic evidence of severe infection (e.g., leukocytosis with left shift or toxic changes, fever, hypoglycemia) should be broad spectrum with good penetration into pancreatic tissue (e.g., enrofloxacin, amoxicillin-clavulanic acid, clindamycin, or ticarcillin-clavulanic acid).

Another aspect of drug therapy for cats with severe pancreatitis is control of nausea and vomiting. In many cats with pancreatitis, vomiting is an uncommon complication; however, it should be controlled in order to improve the animal’s comfort and to allow oral feeding as soon as possible.^3,9 Central-acting antiemetics are the best choices, and they include metoclopramide, ondansetron^g (0.5 to 1.0 mg/kg IV or PO q 24 hours) or dolasetron^h (0.3 to 0.5 mg/kg IV or subcutaneously [SC] q 12 to 24 hours), and chlorpromazineⁱ (0.5 mg/kg SC or IM q 6 to 8 hours). Metoclopramide^j, a dopamine antagonist with both central-and peripheral-acting antiemetic properties, may be administered intermittently (0.2 to 0.4 mg/kg PO or SC q 8 hours) or as a CRI (1 to 2 mg/kg per day or 0.1 to 1.3 μg/kg per minute IV). In addition, metoclopramide is a prokinetic drug that may be beneficial in animals with gastric and duodenal ileus. This drug is readily available and may be adequate in many cats with mild vomiting, but it is not the most potent centrally acting antiemetic and may not be adequate in cats with severe, protracted vomiting. In cats with severe, unremitting episodes of nausea or vomiting, multiple drugs or the use of more potent drugs may be required. The serotonin inhibitors, ondansetron and dolasetron, used alone or together with metoclopramide are often required in these latter cases.

Treatment of the thrombotic complications of pancreatitis should be instituted as needed. Low molecular-weight heparin^k (100 IU/kg SC q 24 hours) has been recommended for prevention of coagulopathies that may occur secondary to SIRS, but no data have been published to document its benefit in cats. In addition, the most appropriate dose and frequency of administration of heparin in cats is unknown. Dopamine^l (5 μg/kg per minute IV) is another drug that has been cited in the treatment of acute pancreatitis in cats, because it may improve pancreatic blood flow and decrease microvascular permeability via stimulation of beta-adrenergic receptors.⁶ Because the effects of dopamine are only beneficial if given in the early hours of pancreatic inflammation (i.e., within 12 hours of onset), and because dopamine may cause nausea and vomiting, it is not recommended in cats. In cats that are persistently hyperglycemic (suggesting glucose intolerance or diabetes mellitus), regular insulin may be initiated (1 U/kg per day IV CRI or 0.2 U/kg IM q 4 to 6 hours).³³ Some cats with severe pancreatic necrosis or recurrent bouts of pancreatitis may develop EPI and subsequently require supplementation with pancreatic enzymes. In these cats, the measurement of serum cobalamin is also indicated, as many of them may require parenteral cobalamin^m (vitamin B₁₂) supplementation (250 μg SC once weekly) indefinitely. In cats with chronic pancreatitis and evidence of concurrent IBD or cholangiohepatitis, corticosteroids may be beneficial.

Dietary Therapy

Foods given to cats with pancreatitis should theoretically be highly digestible, contain moderate to low amounts of fat to reduce pancreatic secretions, and have higher levels of carbohydrates as a calorie source. However, most feline diets are not low in fat, and this approach contradicts their normal diets, which contain few carbohydrates. In one study, some cats with pancreatitis that were fed high-carbohydrate diets became hyperglycemic and developed diarrhea, whereas cats fed higher fat diets tolerated the feeding much better.³⁴ Ultimately, the goal is to find an appropriate diet for the cat that is commercially available, well tolerated by the GI tract, and highly palatable. It is important to note that cats should not be force fed, because it is difficult to achieve the appropriate level of caloric intake by this method, and force feeding can also induce food aversion. In cats with chronic pancreatitis and concurrent IBD, a novel, highly digestible or hydrolyzed diet is often used, similar to those used in the treatment of IBD alone.

Conclusion

Feline pancreatitis is a unique disease compared to its canine counterpart, and it is probably a more frequent problem in cats than was previously known. The combined use of a careful history, subtle evidence of cranial abdominal pain, minimum laboratory data to rule out other causes, a serum fPLI for confirmation of pancreatic inflammation, and changes on abdominal ultrasonography consistent with feline pancreatitis are necessary to make the diagnosis in cats. Medical therapy of pancreatitis in cats is also symptomatic and supportive, but the importance of instituting early and aggressive nutritional support cannot be overstated. Further work is needed to better define the best route for nutritional support (IV versus enteral) and the most effective drugs to control pain and suppress pancreatic inflammation.