For years, feline pancreatitis has been assumed to be a similar disease to that in dogs. Currently, as with so many other disorders, it would appear that this group of disorders is different in the cat. Remembering that the term "pancreatitis" implies nothing more than inflammation of that organ, it is not surprising that each species may have a variety of etiologies.

The incidence of pancreatitis is higher than previously believed. In fact, in a German retrospective study, the prevalence of pathologically significant lesions in dogs was found to be 1.5% and in cats, 1.3% of the specimens submitted. Indeed, there are papers reporting the incidence as high as 2.9 and 3.5% of necropsied cats.

Drs. Joerg Steiner and David Williams classify feline pancreatitis as acute or as chronic. Acute pancreatitis is a short term, completely reversible and without fibrosis on biopsy evaluation. Chronic pancreatitis is a long-term inflammation of the pancreas associated with irreversible histopathological changes, primarily fibrosis. Most of what we see in cats is the latter, which, while not curable, can generally be controlled and has a much lower mortality than severe necrotizing pancreatitis.

Both acute and chronic pancreatitis can be mild or severe, but most commonly, acute cases tend to be more severe, and chronic cases mild. Mild pancreatitis generally results in minimal clinical signs, minimal necrosis, and low mortality.

In severe pancreatitis, (necrotizing, hemorrhagic) extensive pancreatic necrosis and multiple organ involvement +/- organ failure are seen. Fortunately, because in cats this form is rare, severe multi-system complications are uncommon. The prognosis for severe pancreatitis is poor. Complications of acute pancreatitis that may arise include DIC, thromboembolism, cardiac arrhythmia, sepsis, acute tubular necrosis, pulmonary edema, and pleural effusion. It has been suggested that a low dose of dopamine (5 mcg/kg/min) diminishes the severity of the disease. To prevent bacterial translocation, cover these patients with broad-spectrum antibiotics.

Etiology

1.  More than 90% of cases are idiopathic.

2.  Anything causing ischemia to the organ. "The most pivotal determinant in the development and progression of pancreatitis is likely the maintenance of local blood flow. Ischemia favours progression to an autodigestive state; impairment of the microcirculation results in retention of activated enzymes, depletion of anti-proteolytic proteins, and reduced removal of toxic products. Necrosis of the gland follows pancreatic ischemia, leading to a self-perpetuating cycle of damage." (Center SA, Proceedings of AAFP 2000 Fall Meeting)

3.  Several infectious agents have been implicated including feline parvovirus, Toxoplasma organisms (of 45 pancreata examined in 100 cats infected with Toxoplasma, 38 had lesions), feline herpesvirus I, Eurytrema procyonis (a fluke), feline infectious peritonitis (FIP), and, rarely, Amphimerus pseudofelineus. Look for toxoplasmosis.

4.  Other causes include trauma, organophosphate toxicity, and experimentally by infusion of the pancreatic duct with infected fluids. Numerous drugs have been associated with causing pancreatitis in people. NOTE. There is no evidence for glucocorticoids causing acute pancreatitis in dogs or in cats!

Clinical findings

Pancreatitis should be included in a diagnostic rule-out list whenever there is a history of lethargy, anorexia, dehydration, hypothermia, vomiting (in only 35% in one paper), abdominal pain, abdominal mass effect, dyspnea, diarrhea and ataxia. Concurrent problems may include hepatic lipidosis, cholangitis/cholangiohepatitis, idiopathic inflammatory bowel disease, enteritis, diabetes mellitus, and vitamin K1 responsive coagulopathy. As such, the clinical findings on examination may be vague.

Cats diagnosed with hepatic lipidosis and concurrent acute pancreatitis are more likely to be cachectic and have coagulation abnormalities.

Diagnostics

The classical signs of abdominal tenderness or mass in the right anterior quadrant along with haziness in this region and displacement of abdominal viscera on abdominal radio-graphs support the presumptive diagnosis of pancreatitis, however, these findings are uncommon in cats with pancreatitis. Ultrasound is the most sensitive, commonly available, non-invasive evaluative tool that we have at this time. Ultrasonographic findings may include the following changes in the pancreas: swelling, increased echogenicity, mass effects, and fluid accumulation around the pancreas.

Biochemically and hematologically, changes are most commonly mild and non-specific. There may be mild, nonregenerative anemia in chronic pancreatitis or a severe anemia terminally in acute, necrotizing pancreatitis. An inflammatory or stress leukon may be present, and in the case of a pancreatic abscess or a septic suppurative pancreatitis, a left shift may be seen.

Concurrent elevations of sap and alt are not uncommon and reflect inflammatory or lipidotic involvement of adjacent liver. Nonspecific changes, such as hyperglycemia (stress or concurrent diabetes), hypocalcemia, hypokalemia (inappetance), hypercholesterolemia, azotemia (prerenal +/-renal), and hyperbilirubinemia have all been reported.

The lack of sensitivity and specificity of amylase and lipase is a source of frustration in diagnosing feline pancreatitis. A lack of hyperlipasemia cannot be depended on to rule-out pancreatitis. Elevations in serum amylase may occur not only with pancreatitis, but more commonly from other gastrointestinal diseases, as well as from decreased renal clearance of this enzyme.

Trypsin-like immunoreactivity (TLI) has been shown to be diagnostic for severe acute pancreatitis. However, this does NOT detect the more common, chronic and milder forms of pancreatitis. TLI seems most reliable in identifying acute pancreatitis. Later in the course of disease it may not be elevated because either the sick pancreas has leaked all of the enzymes that it had made and isn't capable of producing more (after several days of inflammation) or the pancreatic blood flow has decreased following the worst phase of the inflammatory response. Mild inflammation may also just not stimulate much leakage of enzyme.

Ultimately, surgical biopsy is required to make the histopathological diagnosis. Whilst dogma was that biopsying the pancreas is a pathophysiologically dangerous undertaking, in the cat, this does not appear to be the case.

Gently isolate the pancreas from the surrounding viscera and pack it off with a few gauze swabs prior to selecting either a gross lesion or routine selection of both poles for biopsy using fine iris scissors. Submit a small piece in a culture medium as well as formalin preserved samples, in case the lesion is reported as suppurative.

Therapy

Therapy for pancreatitis is determined by the type of pancreatitis. Fluid therapy and pain relief are the cornerstones in supportive care. Sustain blood and plasma volume, correct acid-base and electrolyte disorders. Concurrent problems (such as lipidosis or enteritis) should be addressed as well. A noteworthy difference between the dog and cat is the recommendation to feed, rather than fast, those patients suspected of (or confirmed as) having pancreatitis unless they are vomiting. Even with the vomiting cat, designing a nutritionally supportive protocol is of great importance due to this species ease of developing lipidosis. Do not fast cats for longer than 48 hours. Use anti-emetics as necessary. In these few intractably vomiting cats, total parenteral nutrition or jejunostomy tube feeding may be advisable for 7-10 days.

Discussion of tube feeding (nasogastric, esophageal, gastrotomy, jejunostomy) may be found in numerous texts.

When the use of anti-emetics is being considered, reduce doses if concurrent liver disease is present. Anti-emetics commonly used in the cat include metoclopramide (Reglan^TM) and chlorpromazine (Largactil^TM). Each of these drugs also has its own, inherent side effects, such as the central nervous system (CNS) sedation or frenzied behaviour or disorientation of Reglan^TM in the cat or the hypotensive effect of the Largactil^TM. Zofran^TM, while costly, is very beneficial in the intractably vomiting patient.

Select Anti-emetics for use in the Cat

It has been suggested that bland, low fat, high carbohydrate diets are most suitable. This author is not aware of any research done to support this recommendation. Cats, being obligate carnivores, don't normally utilize carbohydrates well. Feed a balanced, non protein-restricted diet.

Modification of gastric acidity is advised. An H2 blocker, such as famotidine (0.5 mg/kg IV q12h) or a proton pump inhibitor, such as omeprazole (0.5-1.0 mg/kg PO q24h) may be used.

Analgesia is of critical importance in the comfort of the patient, but also in the progression of the disease/inflammation through the negative physiological effects of pain. Pain causes disease and prevents healing. Even if obvious abdominal pain isn't present, use a "test dose" of 0.1-0.2-mg/kg oxymorphone IV to see if the patient improves over the approximately 6 hour effective period. If that is the case, then constant rate infusion of a narcotic may be considered or a transdermal fentanyl patch (Duragesic^TM) for continuous relief. Torbugesic^TM is not as effective for visceral pain as the opioid agonists are.

Antibiotics are only indicated if the diagnosis of a suppurative pancreatitis or pancreatic abscess has been made. In this case, antimicrobial selection is best made with the knowledge of a sensitivity spectrum. Note that a suppurative pattern may be seen on histology in a sterile pancreatitis caused by enzyme damage.

Corticosteroids and metronidazole are the keys in the long-term treatment for lymphoplasmacytic pancreatitis. Other anti-inflammatories are not currently recommended.

Prognosis

Prognosis depends on the type of pancreatitis involved. Cats with the most common low-grade, chronic lymphoplasmacytic form will live long, comfortable lives with appropriate, long-term therapy.