Until the past ten years pancreatitis was thought to be a mild and uncommon disease in cats. Despite the increasing awareness of pancreatitis in cats, it still remains a difficult disease to diagnose and treatment may be problematic. The histological type that occurs most commonly in cats is chronic non-suppurative pancreatitis (CP). CP usually occurs concurrently with other diseases such as cholangiohepatitis, inflammatory bowel disease and interstitial nephritis, diseases that are often of greater clinical significance.However cats have been increasingly reported to develop acute necrotising pancreatitis similar to dogs, as well as a distinct suppurative form. The acute suppurative form is less common than the necrotising form and tends to affect younger cats. There may be some overlap in histological findings and so generally ANP implies severe disease whilst CP is milder.

Acute necrotising pancreatitis (ANP) in cats is associated with high mortality, as is often the case in canine ANP. However the clinical signs even in a severely affected cat may not be as specific as those expected in dogs with the same condition. 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):

The typical signs such as vomiting and abdominal pain that are usually seen in dogs occur in a much lower percentage of cats with pancreatic necrosis. This is despite the same pathophysiology of pancreatic enzyme activation within the pancreas and subsequent inflammation and necrosis of surrounding tissue. Clinical signs of feline CP are also non-specific and often related to the presence of concurrent disease (e.g., hepatomegaly, thickened intestine). Concurrent disease has been reported in a large number of cats with ANP and up to 100% of cats with chronic pancreatitis.² The most commonly reported organs involved are hepatobiliary (hepatic lipidosis and non-suppurative cholangiohepatitis), renal and gastrointestinal (inflammatory bowel disease). 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.⁴

In order to make a diagnosis of pancreatitis in the cat the clinician usually needs to have a high index of suspicion. Traditional biochemical methods are notoriously non-specific and poorly sensitive at 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 study.³ The underlying cause of hypocalcaemia is not known, but may well be multi-factorial. Measurement of ionised calcium is recommended to avoid false decreases when hypoalbuminemia is present. However, another study showed no difference in ionised calcium between cats with ANP and cats with CP.²

Serum lipase concentration has been shown to increase in cats with experimentally induced acute pancreatitis, although serum amylase remained normal.⁵ 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 right.⁶ A feline trypsin-like immunoreactivity (TLI) assay is available, and has been shown to increase in experimentally induced pancreatitis⁷ 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 CP⁹ to 33% to 66% in both forms^8,10,11 and 80% in ANP,⁹ often dependent on the diagnostic cut-off measurement. TLI measurement may also be increased by other diseases such as renal failure, inflammatory bowel disease, lymphosarcoma and starvation. Unfortunately measurement of trypsinogen activation peptide (and end 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 disease.¹¹

A species specific pancreatic lipase immunoreactivity (fPLI) radioimmunoassay has recently been developed with a reference range established of 1.2-3.8 μg/L.¹² One study showed a very high sensitivity (100%) in 5 cats with ANP, but 54% for the 13 cats with CP.⁹ 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 utility of this test in CP versus ANP, similarly to measurement of cPLI in dogs.

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 of pancreatitis. Classic ultrasound findings of ANP are reported as being similar to that 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 (see table below).

The reason for this discrepancy and lack of sensitivity is unclear, but may reflect the different pathology. Typically, non pancreatic abnormalities are seen in cats with ANP such as a hyperechoic liver, peritoneal effusion and gall bladder distension that may be related to concurrent disease. These may well hamper visualisation of the pancreas. Unfortunately computed tomography (CT) evaluation of the abdomen has so far shown to be of little benefit in cats with acute or chronic pancreatitis.^8,9 This may reflect the lack of infected necroses that occurs in people, or reflect the potential different aetiology and species differences of this disease.

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 of acute suppurative and necrotising pancreatitis is very similar to that for the dog (supportive fluids, analgesia, gastric protectants, anti-emetics). However, as many cats with pancreatitis don't vomit they should be given enteral nutrition as early in the course of the disease as possible to prevent complications such as hepatic lipidosis. Ideally this should happen within the first 24 hours of admission or diagnosis. There is no evidence to suggest that particular food types are more likely to stimulate pancreatic secretion, but it has been suggested that early enteral feeding will reduce cytokine activation. As a general rule, most commercial feline convalescent diet formulations should be adequate for enteral feeding, which often requires assistance via placement of feeding tubes.

Cats with ANP may be more severely affected by hypocalcaemia and so if documented then this should be corrected (50-150 mg/kg IV calcium gluconate over 12-24 hours). Plasma is commonly suggested as beneficial in canine pancreatitis, although definitive studies are lacking. No benefit has been strongly suggested in cats, and generally blood products are used less commonly due to a lack of feline blood products. Other reported treatments such as a dopamine infusion have been shown to have an experimental benefit, but no clinical benefit has been proven.

Antibiotic coverage in dogs with ANP is controversial as bacteria don't seem to play a role in the pathogenesis and progression of disease. However due to the high bacterial count in the feline duodenum and the potential for duodenal reflux to cause the disease, their use is strongly advocated in all cases of ANP and particularly if the acute suppurative form is diagnosed. Empirical choices include amoxicillin or ampicillin, along with metronidazole (although the dose of this should be reduced to 7.5 mg/kg if there is evidence of hepatic dysfunction).

There is some debate about the clinical significance of chronic recurrent pancreatitis in cats. Recent studies suggest that CP may play a role in the development of diabetes mellitus. Unfortunately there is no specific treatment or dietary recommendations that have been substantiated for CP in cats. Generally if there is an underlying disease, then this disease should be treated as the main priority.

The difficulty in non-invasively diagnosing acute pancreatitis in cats has led it to be a disease only recently studied. No specific treatment recommendations can be made based on our current state of knowledge of the naturally occurring disease. However, aggressive supportive therapy is incredibly important to prevent complications and decrease mortality. The reported mortality rate of cats with ANP is high (43%),³ but increases even more so when there is concurrent hepatic lipidosis to 80%.¹⁴ As such, it is strongly recommended that frequent monitoring and early enteral feeding is undertaken in all cats suspected to have ANP.

References

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

2.  Ferreri et al 2003 JAVMA 223:469-478

3.  Kimmel et al 2001 JAVMA 210:1105-1109

4.  Johnston et al 2001 JAVMA 218:48-51

5.  Kitchell et al 1985 AJVR 47:1170-1173

6.  Parent et al 1995 JVIM 9:194

7.  Steiner et al 2000 AJVR 61:620-630

8.  Gerhardt et al 2001 JVIM 15:329-333

9.  Forman et al 2004 JVIM 18:807-815

10. Swift et al 2000 JAVMA 217: 37-42

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

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

13. Saunders et al 2002 JAVMA 221: 1724-1730

14. Akol et al 1993 JVIM 7: 205-209