Feline pancreatitis   see also Pancreas

Pancreatitis is a relatively rare disease in cats. Quite often it is considered in cats with an acute episode of vomiting and often only diagnosed on blood testing.

As in dogs, feline pancreatitis occurs as a result of autodigestion of pancreatic tissue by premature intracellular activation of digestive enzymes such as proteases and phospholipases. This results in local cell damage as well as systemic release of inflammatory cytokines. In cats, 90% of the cases of pancreatitis diagnosed are idiopathic. Pancreatitis in the cat can be acute or chronic as in the dog, but the chronic form is thought to be more common in the cat, and the acute form more common in the dog. Both the acute and the chronic forms can be mild, moderate or severe, further demonstrating the wide spectrum of disease that feline pancreatitis constitutes. Many cases exist concurrently with inflammatory bowel disease, hepatic lipidosis and cholangiohepatitis. Concurrent intestinal and biliary neoplasia has also been reported⁰.

Acute Pancreatitis

Acute pancreatitis is uncommon, but can occur in obese cats that get little exercise and may have eaten a meal with high fat intake. Steroid administration and a decrease in the blood supply to the pancreas each may play a role in the production of acute pancreatitis. When pancreatic cell damage takes place, pancreatic enzymes are released and begin breaking down the fat in other adjacent tissues, resulting in bleeding, shock, endotoxemia (bacterial toxins in the bloodstream), and possibly death.

Pancreatitis can be incredibly challenging to definitively diagnose in cats. The clinical signs in a cat with pancreatitis are vague compared to those seen in a dog with pancreatitis, with lethargy and anorexia most commonly reported. Abdominal pain and vomiting are seen in only 25-52% of affected cats. A complete blood count and blood chemistry profile can be normal, or the findings can be non-specific. Anaemia, leukocytosis, elevation of hepatic enzymes and bilirubin, hypoalbuminemia and hypocalcemia can be seen. Amylase and lipase levels are not useful in diagnosing pancreatitis in the cat. A fairly new assay for fPLI (feline pancreatic lipase immunoreactivity), has been shown to have a sensitivity of 67% and specificity of 91% for diagnosing feline pancreatitis. A similar assay for fTLI (feline trypsin-like immunoreactivity) has been shown to have a lower sensitivity (28%) and specificity (82%).

In one study by Gerhardt in 1999, serum feline trypsin-like immunoreactivity (fTLI) was measured in 21 cats with pancreatitis. The mean fTLI was 127.5 ± 109.5 μg/L (mean ± SD; range, 24–500 μg/L). Fourteen of these 21 cats with pancreatitis had complicating conditions. Their serum fTLI was 153.9 ± 124.3 μg/L (mean ± SD; range, 29–500 μg/L). In this study, abdominal ultrasound showed a sensitivity for pancreatitis of 24%, and abdominal computed tomography had a sensitivity of 20%. Serum fTLI had a sensitivity between 86% when a cut-off value of 49 μg/L was used (upper limit of the control range) and 33% when a cut-off value of 100 μg/L was used.

Many cases are not diagnosed until after the cat's death, when a necropsy (autopsy of an animal) is performed.

Areas of bleeding and necrosis are clearly visible in the body of the pancreas.

Traumatic Pancreatitis

This is usually caused by an accident such as being hit by an automobile, or falling from a height, as in high-rise syndrome. The trauma or injury to the pancreas allows leakage of the enzymes into the surrounding tissues and abdomen, resulting in same clinical picture as in acute pancreatitis.

Chronic Pancreatitis

Chronic pancreatitis usually results from recurrent bouts of acute pancreatitis. It is usually subclinical (symptomless), found at necropsy in older cats. Chronic pancreatitis may lead to diabetes mellitus and exocrine pancreatic insufficiency, but the typical signs of maldigestion are extremely rare in cats. Pancreatic insufficiency results from a decrease or near absence of the digestive enzymes to break down fats, carbohydrates. and proteins, causing malnutrition.

Nodular Hyperplasia

This is a common finding in old cats, at necropsy. It appears as lumps or thickenings in the tissue of the pancreas It is not a malignancy and probably has little clinical significance.

Diagnostic Laboratory Tests

Complete Blood Count (CBC) / Blood Chemistry

Abnormalities detected by standard CBC and blood chemistry analysis are not specific to canine pancreatitis and can be highly variable. A leukocytosis with a left shift is common. Toxic change may be associated with acute pancreatic necrosis. A relative polycythemia or anemia can be seen. Azotemia is a common finding and can be either pre-renal due to dehydration or due to secondary acute renal failure. Liver enzyme activities (ALT, AST, ALP) are often increased, probably due to hepatic ischemia or hepatic damage caused by toxic products from the pancreas. Additional findings include hyperbilirubinemia due to hepatocellular damage or cholestasis, hyperglycaemia caused by hyperglucagonemia, stress, or damage to pancreatic islet cells, hypocalcemia associated with hypoalbuminemia or calcium deposition, hypercholesterolemia, hypertriglyceridemia, and hyperlipidemia.^1,3,5

CBC and chemistry findings in feline pancreatitis are also quite variable and nonspecific. In cats, increased liver enzyme activities can be caused by concurrent hepatic lipidosis or cholangitis/cholangiohepatitis. Hyperbilirubinemia and hyperglycaemia are also commonly seen.^2,3

Amylase and lipase

The activity of serum amylase and lipase can be measured; however, these enzymes do not originate exclusively from the pancreas.⁴ The main sources of serum amylase include the pancreas, liver, and small intestine. Several forms of lipase exist (pancreatic lipase, co-lipase, and lipoprotein lipase) but the pancreas and gastric mucosa are the only known sources.⁷ Regardless of origin, the overall function of amylase and lipase remains the same, meaning that elevations in enzyme activity do not necessarily indicate pancreatic dysfunction .⁴ In the past, these enzymes were used to diagnose canine pancreatitis; however, amylase and lipase have recently been shown to have low sensitivity (62% and 73%,  respectively) and specificity (57% and 55%, respectively).⁴ In one study regarding the utility of amylase and lipase in the diagnosis of feline pancreatitis, no significant difference was found in the serum amylase and lipase activities between cats with acute pancreatitis, cats sick with non-pancreatic disease, and healthy control cats.⁸ Additionally, amylase and lipase can be increased in non-pancreatic diseases such as renal disease (decreased clearance) and gastrointestinal disease. In dogs, corticosteroid administration can cause significant increases in serum lipase.^3,7 Because the level of enzyme activity is not specific to the pancreas, serum amylase and lipase activities are now considered to be of very little value in the diagnosis of pancreatitis in dogs or cats.^1,2

Trypsin activation peptides (TAP)

Trypsin activation peptides (TAP) are the small peptides resulting from the cleavage of trypsinogen to give trypsin. Because trypsinogen should only be activated in the small intestine, TAP is normally absent from or minimally present in the circulating blood. Premature activation of trypsinogen, such as in pancreatitis, can lead to the presence of TAP in serum or urine.⁴ However, serum TAP is not very specific to pancreatitis as it may increase in severe renal disease.^1,7 Additionally, serum TAP may not become increased in mild pancreatitis.⁷ In contrast, urinary TAP is highly specific, but very insensitive.^1,4 To further complicate the issue, TAP is very labile in serum or urine.⁴ Taking into account the cost and limited availability of the test, along with the lack of sensitivity and the labile nature of the peptide, TAP is not considered a clinically useful test for the diagnosis of pancreatitis.¹

Trypsin α-1 proteinase inhibitor complex

As previously mentioned, plasma trypsin α-1 proteinase inhibitor is one of the mechanisms preventing inappropriate activation of trypsinogen. With experimental pancreatitis in dogs, a higher concentration of the inhibitor complex can be found in circulation. However, a significant increase was not found in dogs with spontaneous pancreatitis.⁴ Thus, assays developed to measure trypsin α-1 proteinase inhibitor complex concentration were not found to be clinically useful in the diagnosis of canine pancreatitis.^1,4

Trypsin-like immunoreactivity (TLI)

The trypsin-like immunoreactivity assay is species specific and measures trypsinogen, trypsin and some trypsin molecules bound to proteinase inhibitors. In health, only small amounts of trypsinogen and no trypsin should be present in serum.⁴ Assays for canine TLI (cTLI) and feline TLI (fTLI) are the definitive test for exocrine pancreatic insufficiency.⁹ However, current research on cTLI and fTLI in the diagnosis of pancreatitis indicates the sensitivity is low in both dogs and cats. Steiner et al. reported a sensitivity of 36.4% in the diagnosis of canine pancreatitis.¹⁰ When the recommended cut off of 100μg/L is used to diagnose pancreatitis in cats, the overall sensitivity is low (28 - 33%).^11,12 Feline TLI values are reported to be significantly higher in cats with pancreatitis (mean 100.1 ± 43.0) compared to cats sick with non-pancreatic disease (34.3 ± 4.9) and healthy cats (33.6 ±2.7) according to a study by Parent et al. However, the range of values for cats with pancreatitis (14.8 to 540μg/L) is extensive, meaning that while some cats have significantly elevated TLI values, others have values far below the 100μg/L cut-off.⁸ Overall, the data suggests that serum TLI is not useful in screening dogs or cats for pancreatitis. Although an elevated TLI can be seen with acute pancreatitis, a normal serum TLI does not rule out the presence of pancreatitis.⁹

Pancreatic lipase immunoreactivity (PLI)

While the function of pancreatic lipase is the same as any other lipase in the body, the molecular structure is unique. For this reason, a radioimmunoassay and subsequently an enzyme-linked immunosorbent assay (ELISA) were developed and validated for dogs to measure pancreatic lipase immunoreactivity (cPLI).^13,14 Steiner et al. reported a sensitivity of 81.8% for serum cPLI in the diagnosis of pancreatitis in dogs using a cut off value of 250μg/L.¹⁰ In contrast to serum lipase, cPLI concentration is not affected by decreased glomerular filtration rate or gastritis.⁴ A radioimmunoassay for feline pancreatic lipase immunoreactivity has been developed and validated.¹⁵ In a study of experimentally induced pancreatitis in cats, both serum fTLI and fPLI concentrations increased initially, but fPLI concentrations remained elevated longer.⁴ Forman et al. reported overall sensitivity of 67% and specificity of 91% for fPLI in the diagnosis of pancreatitis.¹¹ Research thus far has indicated that cPLI and fPLI assays are the most sensitive laboratory tests available for the diagnosis of pancreatitis.

Other Diagnostic Tests

Diagnostic imaging

Thoracic and Abdominal radiographs

Thoracic radiographs from patients with pancreatitis are usually normal; however, pleural effusions, oedema and pneumonia have been reported in dogs and cats.^3,4,16 Abdominal radiography has a very low sensitivity for diagnosing pancreatitis. In one retrospective study, abdominal radiographic findings were consistent with a diagnosis of pancreatitis in 24% of 41 cases.⁵ Findings associated with pancreatitis are nonspecific and often absent; however, it remains a useful tool in the work-up of a vomiting dog with abdominal pain or the cat with vague signs of illness. Radiographic signs of pancreatitis include poor serosal detail in the right cranial abdomen, displacement of viscera surrounding the pancreas (stomach to the left, increased angle between pyloric antrum and proximal duodenum, descending duodenum to right, transverse colon caudally), and dilated hypomotile descending duodenum.^1,3,4,17

Abdominal ultrasound

Abdominal ultrasound is highly specific for pancreatitis as long as stringent criteria are applied.^1,11 A retrospective study of canine pancreatitis found ultrasonographic changes consistent with a diagnosis of pancreatitis in 68% of 34 cases of confirmed pancreatitis based upon histopathologic findings.5 Forman et al. reported the sensitivity in cats to be 80% for moderate to severe pancreatitis and 62% for mild pancreatitis (67% overall sensitivity).¹¹ However, other studies have reported lower sensitivities (24 - 35%).^12,16 The normal pancreas can be challenging to identify due to its small size, similar echogenicity to surrounding fat, and lack of a well-defined capsule.¹⁸ Opinions differ as to whether the normal pancreas is visible on ultrasound. A prospective study of 21 client-owned cats with signs consistent with pancreatitis and 8 apparently healthy shelter cats reported the pancreas to be visible in all 8 healthy cats.¹¹ This was in contrast to another study which reported the pancreas to only be visible ultrasonographically in cases that had pancreatic abnormalities.¹⁹ A retrospective study evaluating the use of ultrasound in diagnosing pancreatitis in cats found that the presence or absence of concurrent disease, gross or histologic distribution of pancreatitis, histologic duration, severity and location, clinical suspicion, and operator experience were not associated with ultrasonographic diagnosis of pancreatitis.¹⁶ The use of ultrasound in conjunction with other diagnostic tests can be very useful in the evaluation of pancreatitis.

Computed Tomography

In human medicine, computed tomography (CT) is the most useful imaging modality in diagnosing pancreatitis.¹ One report on the use of CT for diagnosing histologically confirmed canine pancreatitis reported a sensitivity of 64%.20 The reported sensitivity for CT in cats is low (20%).¹² Based on the expense, inconsistent availability, difficulties imaging the feline pancreas and the low sensitivity, CT does not appear to be a clinically useful test in diagnosing feline pancreatitis.

Summary of Diagnostic Testing

Although abnormalities detected on a CBC, blood chemistry profile or abdominal radiographs are typically nonspecific, they are an important part of the work up for potential pancreatitis cases. Measurement of serum amylase and lipase, trypsin activation peptides, and trypsin-like immunoreactivity are of limited use when screening for canine or feline pancreatitis, and if used, should be interpreted in light of their limitations. The most sensitive non-invasive diagnostic test for pancreatitis is the cPLI for dogs and fPLI for cats. Ultrasound is also a useful test that can aid in the diagnosis of pancreatitis. Finally, non-invasive methods for diagnosing pancreatitis require the integration of all available information.

Treatment

Treatment recommendations for feline pancreatitis include supportive fluid therapy, treatment of abdominal pain and cobalamin supplementation if testing reveals a deficiency. Antibiotics and H2-receptor histamine antagonists may or may not be of benefit. In severe, acute pancreatitis, plasma or whole blood therapy is indicated. If chronic pancreatitis exists with inflammatory bowel disease, corticosteroid therapy may be of benefit. In humans, therapy with exogenous pancreatic enzymes results in less abdominal pain. If liver fluke infection is suspected, praziquantel therapy should be given. Low fat diet can be offered, although the role of high fat diet and pancreatitis is not well established in cats. As hepatic lipidosis can occur concurrently in cats with pancreatitis, force feeding or tube feeding is indicated in anorexic cats that are not vomiting. A jejunostomy tube is another feeding option to consider. The prognosis for cats with pancreatitis is quite variable, and depends on the severity of the disease. Acute pancreatitis cats have a poor prognosis and the clinical condition can deteriorate rapidly. Chronic cases tend to have a much better prognosis.

Generally, treatment in dogs and cats is supportive and directed towards restoration of blood volume with intravenous fluids ± colloidal fluids or plasma, controlling vomiting, providing analgesia, and addressing any suspected inciting cause.^1,9 Central acting antiemetics are the treatment of choice for vomiting.⁹ Analgesia is an important component to therapy, even in patients which do not present with obvious abdominal pain.^1,9  Because pancreatitis rarely has infectious components, antibiotics are usually not indicated.¹ Corticosteroid therapy should only be used in cases where the cause is suspected to be autoimmune or in cats with concurrent diseases that warrant corticosteroid treatment (inflammatory bowel disease (IBD), cholangiohepatitis).^1,2,9 Oral intake should be restricted in cases of incessant vomiting for only a short period of time.¹ If a cat is unable to take in oral food or water for more than 2-3 days, other routes of nutrition should be considered to prevent development of hepatic lipidosis and malnutrition.⁹ For dogs or cats, though, enteral nutrition is preferred over parenteral.¹

The prognosis in canine pancreatitis is quite variable and difficult to predict.¹ Some dogs present with an acute fulminating pancreatitis and die regardless of supportive measures. Others can fully recover following an isolated severe event. Chronic or recurrent cases may persist until an acute exacerbation results in death or the animal is euthanized due to poor quality of life and expense of treatment.¹ The prognosis in feline pancreatitis is directly related to the severity of the disease, extent of necrosis, occurrence of systemic or pancreatic complications, duration of disease and presence of concurrent disease.² Additionally, an ionized calcium below 1.00 mmol/L is associated with a 77% mortality rate.²

0. Luther, LE. (2005). http://www.soundvet.com/Pages/Edu/Cases/CS0509.01/Feline_pancreatitis.html

1. Williams DA, Steiner JM. Canine Exocrine Pancreatic Disease. In Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine, Diseases of the Dog and Cat, 6th ed. St. Louis, Elsevier Saunders, 2005, pp. 1482-1487.

2. Steiner JM, Williams DA. Feline Exocrine Pancreatic Disease. In Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine, Diseases of the Dog and Cat, 6th ed. St. Louis, Elsevier Saunders, 2005, pp. 1489- 1491.

3. Simpson, KW. Diseases of the Pancreas. In Tams T. (ed): Handbook of Small Animal Gastroenterology, 2nd ed. St. Louis, W. B. Saunders Co, 2003, pp. 353-365.

4. Steiner JM. Diagnosis of acute pancreatitis. Vet Clin North Am Small Anim Pract 2003; 33: 1181-1195.

5. Hess RS, Saunders HM, Van Winkle TJ, et al. Clinical, clinicopathologic, radiographic, and ultrasonographic abnormalities in dogs with acute pancreatitis: 70 cases (1986-1995). J Am Vet Med Assoc 1998 Sep1; 213(5): 665-70.

6. Hill RC, Van Winkle TJ. Acute necrotizing pancreatitis and acute suppurative pancreatitis in the cat. A retrospective study of 40 cases (1976-1989). J Vet Intern Med 1993; 7: 25-33.

7. Bounous, DI. Digestive System. In Latimer KS, Mahaffey EA, Prasse KW (eds): Clinical Pathology, 4th ed. Ames, Iowa, Iowa State Press, 2003, pp. 215-219.

8. Parent CR, Washabau J, Williams DA, et al. Serum trypsin-like immunoreactivity, amylase and lipase in the diagnosis of feline acute pancreatitis. J Vet Intern Med 1995; 9: 194 (abstract).

9. Zoran DL. Pancreatitis in Cats: Diagnosis and Management of a Challenging Disease. J Am Anim Hosp Assoc 2006; 42:1-9.

10. Steiner JM, Broussard J, Mansfield CS, et al. Serum canine pancreatic lipase immunoreactivity (cPLI) concentrations in dogs with spontaneous pancreatitis. J Vet Intern Med 2001; 15:274 (abstract).

11. Forman MA, Marks SL, De Cock HEV, et al. Evaluation of Serum Feline Pancreatic Lipase Immunoreactivity and Helical Computed Tomography versus Conventional Testing for the Diagnosis of Feline Pancreatitis. J Vet Intern Med 2004;18:807-815

12. Gerhardt A, Steiner JM, Williams DA, et al. Comparison of the sensitivity of different diagnostic tests for pancreatitis in cats. J Vet Intern Med 2001;15:329-333.

13. Steiner JM, Williams DA. Development and validation of a radioimmunoassay for the measurement of canine pancreatic lipase immunoreactivity (cPLI) in serum. J Vet Intern Med 2000;14:378 (abstract).

14. Steiner JM, Teague SR, Williams DA. Development and analytic validation of an enzyme-linked immunosorbent assay for the measurement of canine pancreatic lipase immunoreactivity in serum. Can J Vet Res 2003;67:175-182.

15. Steiner JM, Wilson BG, and Williams DA. Development and analytic validation of a radioimmunoassay for the measurement of feline pancreatic lipase immunoreactivity in serum. Can J Vet Res 2004;68:309-314.

16. Saunders HM, Van Winkle TJ, Drobatz K, et al. Ultrasonographic findings in cats with clinical, gross pathologic, and histologic evidence of acute pancreatic necrosis: 20 cases (1994-2001). J Am Vet Med Assoc 2002;221:1724-1730.

17. Steiner JM, Broussard J, Mansfield CS, et al. Serum canine pancreatic lipase immunoreactivity concentrations in dogs with spontaneous pancreatitis. J Vet Intern Med 2001;15:274 (abstract).

18. Mahaffey MB, Barber DL. The peritoneal space. In Thrall DE (ed): Textbook of veterinary diagnostic radiology, 4th ed. Philadelphia, Elsevier Saunders, 2002, pp. 516-539.

19. Swift NC, Marks SL, MacLachlan NJ, Norris CR. Evaluation of serum feline trypsin-like immunoreactivity for the diagnosis of pancreatitis in cats. J Am Vet Med Assoc 2000;217: 37-42.

20. SpillmanT, Litzlbauer H, Moritz A, et al. Computed tomography and laparoscopy for the diagnosis of pancreatic diseases in dogs. Proceedings of the 18th ACVIM forum. Seattle, WA, 2000:485-487 (abstract).