Pancreatitis in Cats
World Small Animal Veterinary Association World Congress Proceedings, 2004
David A. Williams, MA VetMB, PhD, MRCVS, DACVIM, DECVIM-CA
Gastrointestinal Laboratory
College Station, TX, USA

Clinical signs in patients with pancreatitis vary enormously depending on the severity of the disease. Cats, even with severe pancreatitis, present with less specific clinical signs than do dogs. In one study of 40 cats with severe pancreatitis the following clinical signs were reported: lethargy (100%), anorexia (97%), dehydration (92%), hypothermia (68%), vomiting (35%), abdominal pain (25%), a palpable abdominal mass (23%), dyspnea (20%), ataxia (15%), and diarrhea (15%). Clinical signs in patients with pancreatitis are due to pancreatic inflammation or due to systemic complications. Until recently it was believed that systemic signs commonly seen in pancreatitis patients, like local effects, are a direct result of circulating pancreatic enzymes. While there is little doubt that some of these systemic effects, such as systemic lipodystrophy, are caused by circulating pancreatic enzymes, recent data would suggest that other systemic sequelae are a consequence of the release of inflammatory mediators released into the vascular space in response to pancreatic inflammation. A systemic inflammatory response, consisting of release of neutrophils from the bone marrow, chemotaxis of leucocytes, and degranulation of mast cells, basophils, and eosinophils, and platelet aggregation occur commonly in patients with severe forms of pancreatitis and can lead to fever. Other systemic effects seen in patients with severe pancreatitis are systemic vasodilation leading to hypotension and sometimes acute renal failure, pulmonary edema leading to respiratory failure, disseminated intravascular coagulation, and in some cases multi-organ failure. A few patients also develop systemic lipodystrophy, also known as pancreatitis associated panniculitis. Neurologic signs such as disorientation have been seen in human, canine, and feline patients with severe pancreatitis and are sometimes referred to as pancreatic encephalopathy. No clinical signs are specific for pancreatitis in cats, and vomiting and cranial abdominal pain are far less common in cats than in dogs.


In one study of cats with severe pancreatitis findings included anemia (26%), hemoconcentration (13%), leucocytosis (30%), and leukopenia (15%).1 A routine serum chemistry profile may show mild elevations of hepatic enzymes. Electrolyte abnormalities are commonly seen in severe cases. Azotemia maybe seen reflecting either dehydration, or more rarely acute renal failure secondary to pancreatitis. Hypoalbuminemia is common, as is hypocalcemia, which may be secondary to hypoalbuminaemia, or to formation of calcium salts with fatty acids. Urinalysis often reveals an elevated urine specific gravity secondary to dehydration. In the severe cases acute renal failure may ensue and the urine specific gravity may drop and casts maybe seen in the sediment. None of the findings is specific. These tests are nonetheless important because they more serve to rule out disorders other than pancreatitis and to assess the overall status of the patient.


Abdominal radiographs may show a loss of detail in the cranial abdomen. In some cases there maybe a suggestion of a mass in the cranial abdomen. Transposition of abdominal organs can also be seen in some cases and may include a transposition of the duodenum dorsally and laterally, the stomach to the left, and the transverse colon caudally. However, these findings are rather subjective and a conclusive diagnosis of pancreatitis is not possible by abdominal radiography alone.

In contrast, abdominal ultrasonography is highly specific for pancreatitis if stringent criteria are applied. An enlarged pancreas alone is not sufficient to make a diagnosis of pancreatitis since pancreatic edema can also be observed with portal hypertension or hypoalbuminemia. The pancreas may appear hypoechoic when pancreatic necrosis is present and may appear hyperechoic in cases where pancreatic fibrosis has developed. In acute cases a hypoechoic pancreas is often surrounded by a hyperechoic area that is due to peripancreatic fat necrosis. Chronic pancreatitis can be associated with a hyperechoic pancreas indicating the presence of pancreatic fibrosis. Finally, pancreatitis is often associated with various degrees of peripancreatic fluid accumulation. The sensitivity of this diagnostic modality in low in cats, however, ranging between 11 and 25%.

Contrast-enhanced abdominal computed tomography is the diagnostic tool of choice for human patients suspected of having pancreatitis. This technology is not only highly sensitive for a diagnosis of pancreatitis but is also a sensitive tool for the detection of pancreatic necrosis and thus is useful as a diagnostic as well as a prognostic tool. However, a recent study showed that contrast-enhanced abdominal computed tomography was inferior to abdominal ultrasonography in cats with suspected pancreatitis.


A pancreatic biopsy is the definitive diagnostic method for pancreatitis. Pancreatic biopsies can be collected during abdominal exploratory or by laparoscopy. Pancreatitis may be grossly apparent in some cases. However, the absence of pancreatitis can be difficult to prove. Affected areas may be grossly inapparent, and unless multiple biopsies from different sites are taken pancreatitis cannot be conclusively excluded. It should also be noted that while a pancreatic biopsy in itself is associated with very few complications and is considered safe, many patients with pancreatitis are a poor anesthetic risk prior to medical stabilization.


Serum lipase and amylase activities have been shown to be of no clinical usefulness for the diagnosis of pancreatitis in cats. Current evidence suggests that when values of these enzymes in feline serum are increased, the underlying disease is not present in the pancreas. Many such cats have chronic small intestinal disease and / or gastritis.

Serum feline trypsin-like immunoreactivity (fTLI) has been shown to be specific for exocrine pancreatic function in cats. Cats with experimental pancreatitis have increased serum TLI concentrations, although the increases generally last only a few days. Some 30-60% of cats with spontaneous pancreatitis have increased serum TLI concentration. Serum fTLI can increase in cats with moderate to severe renal dysfunction, but is by far the most sensitive diagnostic test for feline pancreatitis reported in the literature to date.

Recently, a new assay for the measurement of pancreatic lipase in cats (fPLI) has been developed. Preliminary results indicate that, as for the corresponding assay in dogs, measurement of serum fPLI concentration is both more sensitive and specific than any other diagnostic tool for the diagnosis of feline pancreatitis. Assays of both fTLI and fPLI are currently available from the author's laboratory.


The treatment of acute pancreatitis involves maintenance of fluid and electrolyte balance while removing the cause of the pancreatitis, if known, thereby allowing the pancreas to recover from the inflammatory episode. Since most cats with pancreatitis are anorexic, withholding food not useful, and indeed nutritional support is generally given by enteral means (esophagostomy or gastrostomy feeding tube) to prevent (or treat) concurrent hepatic lipidosis. There is no clinical impression that such enteral nutrition exacerbates the course of pancreatitis, and in fact cats clearly do better overall when nutritional support is given.

If drug-induced pancreatitis is suspected then any incriminated agents should be withdrawn and replaced by an unrelated alternative drug if necessary. Other potential etiologic factors should similarly be investigated, and if possible rectified. Some patients require aggressive fluid therapy over several days to treat severe dehydration and ongoing fluid electrolyte loss due to vomiting and diarrhea. Many animals become hypokalemic during such therapy and serum potassium should be monitored and supplemented as needed by addition of potassium chloride to the IV fluids. Serum creatinine or BUN should also be followed to monitor renal function. While metabolic acidosis is probably common in acute pancreatitis, this may not always be the case and vomiting patients may be alkalotic. Blind correction of suspected acid base abnormalities should therefore not be attempted. Excessive bicarbonate administration may precipitate signs of hypocalcemia in individuals with borderline low calcium levels.

It is common practice to give parenteral antibiotics during this supportive period, particularly when toxic changes are evident in the hemogram or when the patient is febrile. However, in contrast to human patients with pancreatitis, feline patients with pancreatitis rarely have infectious complications and antibiotic therapy may thus not be warranted. In addition, several antibiotic agents have been implicated in causing pancreatitis (notably tetracyclines in cats) and in any case their use may also predispose patients to secondary infections with antibiotic-resistant organisms.

If abdominal pain is suspected analgesic therapy (morphine, fentanyl, butorphanol by constant rate infusion, repeated IV, IM, or SQ injection, or dermal patch) should be given as needed to provide relief. Many cats with pancreatitis will not show clear evidence of abdominal discomfort but may benefit significantly from analgesic therapy. The author suggests analgesic therapy in all cats with pancreatitis. If there is no apparent improvement in overall attitude, analgesic therapy can be discontinued.

Hyperglycemia is often mild and transient, but in some cases frank diabetes mellitus may develop and may require treatment with insulin. Respiratory distress, neurologic problems, cardiac abnormalities, bleeding disorders, and acute renal failure are all poor prognostic signs.

In severe acute pancreatitis there is marked consumption of plasma protease inhibitors as activated pancreatic proteases are cleared from the circulation. Saturation of available α-macroglobulins is rapidly followed by acute disseminated intravascular coagulation, shock, and death. Transfusion of plasma or whole blood to replace α-macroglobulins may be life-saving in these circumstances, and has the additional benefit of maintaining plasma albumin concentrations. Albumin is probably beneficial in pancreatitis because of its oncotic properties that not only help maintain blood volume and prevent pancreatic ischemia, but also limit pancreatic edema formation. Albumin also binds detergents such as free fatty acids and lysolecithin, produced in pancreatitis by the catalytic actions of lipase and phospholipase A2, that otherwise may disrupt cell membranes. While plasma administration has not been shown to be beneficial in human patients with pancreatitis, it is the author's clinical impression that plasma has ameliorating effects in feline patients with severe pancreatitis.

Low molecular weight dextrans have also been used to expand plasma volume, but they may aggravate bleeding tendencies, contain no protease inhibitor, and provide no major advantages over plasma administration. In one experimental study a hypertonic saline-dextran 70 combination was effective in maintaining cardiac function while avoiding massive fluid administration and avoiding pulmonary hypertension and edema that can accompany therapy with lactated Ringer's solution alone. Hyperoncotic ultrahigh molecular weight dextran solutions have recently been shown to reduce trypsinogen activation, prevent acinar necrosis, and lower mortality in rodent pancreatitis, perhaps by promoting pancreatic microcirculation.

Small amounts of water should be offered after the patient has stopped vomiting. If there is no recurrence of clinical signs, food may be gradually re-introduced. The role of high fat content diets in promoting feline pancreatitis is not known, and may be less important than in dogs. While the prognosis is poor for those patients that repeatedly cannot tolerate food, total parenteral nutrition may be beneficial by sustaining such patients while the digestive system is rested for 7-10 days. In many patients a single episode of pancreatitis occurs, and all that is necessary in the way of long-term therapy is to avoid any known or potential predisposing factors. In other patients repeated bouts of pancreatitis occur, sometimes with concurrent disease in other locations.

Peritoneal dialysis to remove toxic material accumulated in the peritoneal cavity is beneficial experimentally, and is thought by many to be useful in human patients. While impractical in some veterinary hospitals, peritoneal dialysis may be of value in some cases. Certainly in those patients in which acute pancreatitis is confirmed at exploratory laparotomy, removal of as much free fluid as possible by abdominal lavage is advisable. In some cases pancreatitis may be localized to one lobe of the gland, and surgical resection of the affected area may be followed by complete recovery.

Use of corticosteroids in acute pancreatitis has been recommended because they stabilize lysosomal membranes, reduce inflammation and alleviate shock, but they have not been shown to be of value in experimental studies. They should be given only on a short-term basis to animals in shock associated with fulminating pancreatitis, and then in concert with fluids and plasma as described above. Longer periods of administration may impair removal of α-macroglobulin-bound proteases from the plasma by the monocyte-macrophage system, with resultant complications due to systemic effects of circulating uninhibited enzymes.

Recent studies have identified human patients with glucocorticoid responsive immune-mediated pancreatitis. There is a chronic form of pancreatitis in cats that often occurs with concurrent lymphocytic plasmacytic enteritis, and administration of prednisolone to many of these patients improves clinical signs. However it is not know if the pancreatic pathology, intestinal pathology, or both, are responding to this treatment. Traditionally, glucocorticoids have been believed to be a risk factor for pancreatitis in human beings. However, recently it was postulated that this suspicion was based on statistical bias and glucocorticoids have now been removed from the list of drugs that are believed to be risk factors for pancreatitis.

Numerous other treatments have been proposed to be potentially useful based on experimental studies, but have not been effective in human patients and cannot be recommended in cats These include naloxone, dopamine, nasogastric suctioning of gastric secretions, antacids, cimetidine, atropine, acetazolamide, glucagon, calcitonin, somatostatin and its analogues, a variety of naturally occurring and synthetic enzyme inhibitors, anti-oxidant agents and free-radical scavengers including vitamin E, selenium, and S-adenosyl methionine.

Future clinical and experimental trials will probably be directed at the use of agents to modify cellular events that are currently believed to be important in the pathobiology of pancreatitis. Recent findings about the importance of inflammatory cytokines in the progression of pancreatitis and the development of complications has led to new efforts to utilize antagonists and modifiers of inflammatory cytokines to treat pancreatitis. Despite these initially promising results none of these agents has achieved clinical significance in human medicine. However, further studies in this field can be expected over the next few years.

In mild, as in severe cases of pancreatitis, some effort should be directed at identifying the cause of pancreatitis, such as hypertriglyceridaemia or hypercalcemia. Cats with chronic pancreatitis can be treated with praziquantel for possible hepatic flukes causing pancreatitis, which, while rare, is treatable. Oral pancreatic enzymes are commonly given to human patients with chronic pancreatitis, and while this does not relieve inflammation it does seem to reduce abdominal pain in some patients. Finally, since in some cats pancreatitis is subclinical, no therapy may be required. However, consideration should be given to possible future complications such as diabetes mellitus, exocrine pancreatic insufficiency, or clinical pancreatitis.

Speaker Information
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David A. Williams, MA VetMB, PhD, MRCVS, DACVIM, DECVIM-CA
Gastrointestinal Laboratory
College Station, TX

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