Can We Diagnose Feline Pancreatitis and Do We Need To?
World Small Animal Veterinary Association World Congress Proceedings, 2008
Caroline Mansfield, BSc, BVMS, MACVSc, MVM, DECVIM-CA
Department of Veterinary Clinical Sciences, Murdoch University
Western Australia, Australia

Pancreatitis in the cat is still poorly understood, and diagnosed much less commonly, than pancreatitis in the dog. This may not reflect the true incidence of the disease, rather the vague clinical presentations and lack of accurate diagnostic tests that make it exceptionally difficult to determine. A recent survey of 115 feline post-mortems at a tertiary referral institution found that there was an overall prevalence of 67% for pancreatitis, with 45% of clinically healthy cats also having pancreatic lesions1.

Part of the difficulty with feline pancreatitis is that chronic non-suppurative pancreatitis (CP) is the histological type that occurs most commonly in cats. CP usually occurs concurrently with other diseases such as cholangiohepatitis, inflammatory bowel disease and interstitial nephritis, diseases that may be of greater clinical significance. This form has a fair degree of fibrosis with minimal inflammation, and histopathology remains the gold standard method for diagnosis. However cats have been increasingly reported to develop acute necrotising pancreatitis (AP) similar to dogs, with necrosis of the peri-pancreatic fat region being a predominant feature. Again, about 2/3 of cats in a recent survey with AP had concurrent disease1. There also appears to be a acute suppurative form that is unique to cats. This type is uncommon and tends to affect younger cats. A possible auto-immune form with periductular lymphocytic inflammation has also been described1.

Clinical Signs

AP in cats is associated with high mortality2-4. However the clinical signs even in a severely affected cat are not particularly specific for pancreatitis, and often reflect concurrent pathology. Concurrent disease has been reported in a large number of cats with AP and up to 100% of cats with CP3. The most commonly reported organs involved are the hepatobiliary (hepatic lipidosis and non-suppurative cholangiohepatitis), renal and intestinal (inflammatory bowel disease) systems. This is most likely related to the unique anatomy of the feline pancreatic and biliary duct system, as well as the higher intestinal bacterial count in cats5. Three studies in the past 15 years confirm this, as do several smaller case series. The following table summarises the main clinical findings (NR= not reported):

Table. Clinical signs in feline acute pancreatitis.

Clinical sign

Hill & Van Winkle 19932

Kimmel et al 20014

Ferreri et al 20033

Case numbers

n = 40 AP
(necropsy based)

n = 46 AP

n = 30 ANP

n = 33 CP

Lethargy

100%

83%

50%

52%

Anorexia

97%

96%

63%

70%

Dehydration

92%

NR

33%

51%

Hypothermia

68%

NR

NR

NR

Vomiting

35%

43%

43%

39%

Abdominal pain

25%

17%

10%

Palpable abdominal mass

23%

4%

3%

Diarrhoea

15%

11%

NR

NR

Dyspnoea

20%

NR

16%

Ataxia

15%

NR

NR

NR

Weight loss

NR

39%

40%

21%

Jaundice

NR

22%

16%

24%

Pallor

NR

NR

30%

30%

Diagnosis

Traditional biochemical methods are notoriously non-specific and poorly sensitive for diagnosing any pancreatic inflammation in the cat and changes generally reflect concurrent disease and the electrolyte/fluid imbalances caused by the disease. They are however important to perform in order to obtain basic information to direct fluid and electrolyte therapy and assess for evidence of concurrent disease. The presence of hypocalcaemia has been shown to be a poor prognostic indicator in cats, even in the absence of clinical signs associated with hypocalcaemia in one study4. The underlying cause of hypocalcaemia is not known, but may well be multi-factorial. Measurement of ionised calcium is recommended. However, another study showed no difference in ionised calcium between cats with ANP and cats with CP3.

Serum lipase concentration has been shown to increase in cats with experimentally induced acute pancreatitis, although serum amylase remained normal6. The increase in serum lipase and amylase in cats tends to be much less in pancreatitis than in the dog and these values are seldom diagnostic in their own right7.

An assay for feline trypsin-like immunoreactivity (fTLI) is available, and this has been shown to increase in experimentally induced pancreatitis8 but unfortunately it is not always increased at the time of clinical diagnosis. There is a range of reported sensitivity for fTLI from 8% in CP10 to 33% to 66% in both forms9,11,12 and 80% in ANP10, often dependent on the diagnostic cut-off value used. Concentration of fTLI may also be increased by other diseases such as renal failure, inflammatory bowel disease, lymphosarcoma and starvation. Unfortunately measurement of trypsinogen activation peptide (a by-product cleaved by trypsin activation) is no more sensitive or specific than measurement of fTLI and as it is not readily available is of little benefit in diagnosing this disease12.

A species specific pancreatic lipase immunoreactivity (fPLI) radioimmunoassay has recently been developed with a reference range established of 1.2-3.8 µg/L13. One study showed a very high sensitivity (100%) in 5 cats with ANP, but 54% for the 13 cats with CP for this test10. Overall the specificity of fPLI in that study (compared to 8 healthy cats and 3 symptomatic cats with normal pancreatic histopathology) was 91%, which shows there may be minimal effects from other diseases. Once larger studies have been published the true sensitivity and specificity of this test can be established. However, it does appear as if there may well be a difference in the diagnostic usefulness of this test in CP versus AP.

Feline pancreatitis is difficult to assess via diagnostic imaging. Abdominal radiographs tend to be non-helpful, particularly in CP, although they may be useful to assess for other abdominal disease. The increased availability of ultrasound has made this a commonly used method of ante-mortem diagnosis in cats, but it should not be relied on to exclude a diagnosis, particularly of CP. Classic ultrasonographic findings of AP are reported as being similar to those in dogs (enlarged hypoechoic pancreas with hyperechoic peri-pancreatic tissue). Despite an increase in operator expertise, some studies have shown a very disappointing sensitivity for the diagnosis of pancreatitis (particularly the chronic form) in cats. It has also been shown that pancreatic duct dilatation, once considered a hallmark of CP, may be an age-related change and not reflect inflammation14,15. Endosonography may have no advantage over trans-abdominal ultrasound, except perhaps in obese cats16. Unfortunately computed tomography (CT) evaluation of the abdomen has so far been shown to be of little benefit in cats with acute or chronic pancreatitis9,10, but scintigraphy using radio-labelled leucocytes may offer an alternative diagnostic modality17.

In many cases the diagnosis can only be made on histological evaluation of the pancreas. Surgical exploration may be contraindicated in severely unwell animals, but full evaluation of the abdomen and sampling from the liver and intestine may result in a complete diagnosis and assessment of concurrent disease. Pancreatic biopsies per se are not necessarily deleterious but decreased blood flow or hypotension during general anaesthesia may worsen or precipitate inflammation of the organ.

Treatment

There is no specific treatment for feline CP, and treatment of the underlying disease remains the most imperative. This may beg the question of how vital it is to diagnose CP in cats. As we currently do not know the role CP has in perpetuating or worsening prognosis with IBD and cholangiohepatitis, we cannot answer at this point in time. The potential to cause a sub-set of diabetes mellitus is also worthy of further investigation, as is the possibility of an immune-mediated aetiology.

References

1.  De Cock, et al. 2007 Vet Path 44:39-49

2.  Hill & Van Winkle, 1993 JVIM 7:25-33

3.  Ferreri, et al. 2003 JAVMA 223:469-478

4.  Kimmel, et al. 2001 JAVMA 210:1105-1109

5.  Johnston, et al. 2001 JAVMA 218:48-51

6.  Kitchell, et al. 1985 AJVR 47:1170-1173

7.  Parent, et al 1995 JVIM 9:194

8.  Steiner, et al. 2000 AJVR 61:620-630

9.  Gerhardt, et al. 2001 JVIM 15:329-333

10. Forman, et al. 2004 JVIM 18:807-815

11. Swift, et al. 2000 JAVMA 217: 37-42

12. Allen, et al. Can J Vet Res 2006; 70: 313-316

13. Steiner, et al. Can J Vet Res 2004; 68:309-314

14. Hecht, et al. 2006 Vet Rad US 47:287-294

15. Larson, et al. 2005 Vet Rad US 46:238-242

16. Schweighauser, et al. 2006 JVIM 20:750 (abstract)

17. Head, et al. 2005 Vet Rad US 46:263-266

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Caroline Mansfield, BSc, BVMS, MACVSc, MVM, DECVIM-CA
Department of Veterinary Clinical Sciences
Murdoch University
Murdoch, Western Australia, Australia


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