Journal of Feline Medicine and Surgery

http://jfm.sagepub.com/

Pancreatitis in cats: Is it acute, is it chronic, is it significant?

Julien Bazelle and Penny Watson
Journal of Feline Medicine and Surgery 2014 16: 395
DOI: 10.1177/1098612X14523186

The online version of this article can be found at:

http://jfm.sagepub.com/content/16/5/395

Disclaimer

The Journal of Feline Medicine and Surgery is an international journal and authors may discuss products and
formulations that are not available or licensed in the individual reader's own country.
Furthermore, drugs may be mentioned that are licensed for human use, and not for veterinary use. Readers need to
bear this in mind and be aware of the prescribing laws pertaining to their own country. Likewise, in relation to
advertising material, it is the responsibility of the reader to check that the product is authorised for use in their own
country. The authors, editors, owners and publishers do not accept any responsibility for any loss or damage arising
from actions or decisions based on information contained in this publication; ultimate responsibility for the treatment of
animals and interpretation of published materials lies with the veterinary practitioner. The opinions expressed are those
of the authors and the inclusion in this publication of material relating to a particular product, method or technique does
not amount to an endorsement of its value or quality, or the claims made by its manufacturer.

Published by:
International Society of Feline Medicine

American Association of Feline Practitioners

and
http://www.sagepublications.com

Additional services and information for Journal of Feline Medicine and Surgery can be found at:

Email Alerts: http://jfm.sagepub.com/cgi/alerts

Subscriptions: http://jfm.sagepub.com/subscriptions

Reprints: http://www.sagepub.com/journalsReprints.nav

Permissions: http://www.sagepub.com/journalsPermissions.nav

>> Version of Record - May 2, 2014

What is This?

Downloaded from jfm.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 2, 2014

Journal of Feline Medicine and Surgery (2014) 16, 395–406

CLINICAL REVIEW

PANCREATITIS IN CATS
Is it acute, is it chronic,
is it significant?
Julien Bazelle and Penny Watson

Feline pancreatitis has been recognised for more than 40 years.1,2 Despite
marked improvement in our understanding of the disease, and develop-
Practical relevance: Pancreatitis is

ment of more sensitive and specific diagnostic tools, many questions

a frequent finding in cats, the chronic

on the pathophysiology of feline pancreatitis remain unanswered. This

form being more common than the acute

article sets out to review current knowledge on the aetiology, diagnosis

form. Despite the large number of

and treatment of feline pancreatitis, and to determine the clinical signif-

diseases or conditions that may be

icance of this particularly challenging disease.

associated with feline pancreatitis, in most
cases no cause is diagnosed and the pancreatitis
is said to be idiopathic. The chronic form can be
What are the different forms of pancreatitis mild and asymptomatic, and has a high prevalence
in cats? in apparently healthy cats. This has generated

Pancreatitis is an inflammatory disease of the exocrine pancreatic

debate concerning the clinical significance of

tissue and can be divided into acute and chronic types based on histo-
chronic feline pancreatitis. However, several reports

logical findings.3,4 Until recently, pathological classification of feline

have demonstrated the severity of clinical signs in

pancreatitis was based on the human classification system.5 In 2007,

certain forms of acute feline pancreatitis, while

the histopathological characteristics of feline pancreatitis were

other studies have reported a strong association

reviewed and a scoring system was designed to grade the severity of

between chronic pancreatitis and the development

pancreatitis.6 Two main forms of feline pancreatitis have been

of comorbidities such as hepatic lipidosis, diabetes

described. Acute pancreatitis (AP) is characterised by neutrophilic

mellitus, inflammatory bowel disease or exocrine

inflammation and varying amounts of pancreatic acinar cell and peri-

pancreatic insufficiency. This suggests that feline

pancreatic fat necrosis (Figure 1).6 Chronic non-suppurative pancreati-

pancreatitis should not be overlooked.
Clinical challenges: Diagnosis of feline
pancreatitis is complicated by the non-specific
clinical signs and poor diagnostic value of basic
biochemistry and haematology or imaging
techniques. Development of a feline-specific
pancreatic lipase immunoassay has improved our
diagnostic ability in the past decade, but may have
more limited application for mild and chronic forms
of pancreatitis. Moreover, histopathology (the ‘gold
standard’ diagnostic test) can be associated with
false-negative results due to multifocal distribution
Figure 1 Histological
section of the pancreas of lesions or mild forms of the disease. With respect
of a cat with acute to treatment, it is important to take into account the
pancreatitis. Note the
intense peripheral fat
idiosyncrasies of the feline species when
necrosis and infiltration considering medical therapies.
by mononuclear cells.
Evidence base: This article reviews the literature
Haematoxylin and eosin
(H&E) x 40 on feline pancreatitis, focusing on the different
forms and their relative clinical significance,
Julien Bazelle while explaining difficulties inherent in the
DVM MRCVS*
Willows Veterinary Centre and Referral Service, diagnosis of this disease. An overview of current
Shirley, Solihull, West Midlands, B90 4NH, UK recommendations for the management of cats
Penny Watson with pancreatitis is also provided.
MA VetMD CertVR DSAM DipECVIM MRCVS
Queen’s Veterinary School Hospital,
University of Cambridge, Madingley Road,
Cambridge CB3 0ES, UK
*Corresponding author: julien.bazelle@willows.uk.net

DOI: 10.1177/1098612X14523186
© ISFM and AAFP 2014 Downloaded from jfm.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 2, 2014 JFMS CLINICAL PRACTICE 395
R E V I E W / Pancreatitis in cats – what’s the clinical significance?
How prevalent is feline pancreatitis?
Information on the prevalence of pancreatitis in cats is scarce.
Reported prevalence based on histopathological findings
ranges between 0.6% and 67%,1,6,9 and this marked variance
may reflect differences in study populations or study design
(eg, histological diagnostic criteria). One study revealed that
typical lesions of both acute and chronic forms of pancreatitis
are often multifocal, underlining the need to examine multiple
sections of the pancreas.6 However, this is of course not
practical or advisable in the clinical setting, unless post mortem
material is available. The same study also emphasised the fact
that many patients with CP have only mild histological changes,
which may account for the high prevalence found compared with
previous studies.6
Most of the case series published to date have reported a
tis (CP) is characterised by lymphocytic inflam-
mation, fibrosis and acinar atrophy (Figure 2).6
An earlier study divided AP into two forms:
‘acute necrotising’, where there was signifi-
cant fat necrosis, and ‘acute suppurative’,
where fat necrosis was not a significant fea-
ture.7 The authors of that study also included
some cases with concurrent interstitial fibrosis
and lymphocytes and plasma cells (findings
that are consistent with more chronic changes)
in the acute necrotising group.7 This demon-
strates that, unfortunately, there is some over-
lap between AP and CP histologically and it
has been suggested that these represent differ-
ent points on a disease continuum.8
Pancreatitis is an inflammatory disease
of the exocrine pancreatic tissue and
can be divided into acute and chronic types
based on histological findings.
a b
Figure 2 Histological sections of the pancreas of a cat with chronic
pancreatitis, at x 10 (a) and x 40 (b) magnification. Note the extensive fibrous
tissue (pale pink) surrounding and disrupting darker pink acinar tissue and
clumps of lymphoplasmacytic inflammation (dark purple) at the top and bottom
of section (a). H&E
396 JFMS CLINICAL PRACTICEDownloaded from jfm.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 2, 2014
higher frequency of CP compared with AP in cats.1,6,10,11 One
study found similar prevalences of CP and AP based on histol-
ogy; however, it was noted that some histological findings like
fibrosis or necrosis could be shared by AP and CP patients.8 This
tends to suggest that there is some overlap between acute and
chronic forms of feline pancreatitis.
Despite its frequency, definitive diagnosis of feline pancreatitis
is rarely achieved ante mortem.6,9,12 The high frequency of mild
CP reported in some studies, even in healthy patients,6 does
raise the question about the clinical significance of mild lesions.
However, the discrepancy between the prevalence of histological
lesions and the frequency of ante-mortem diagnosis probably
also indicates that some clinically significant pancreatitis
escapes diagnosis in cats.
Why is feline pancreatitis
so overlooked?
Diagnosing feline pancreatitis ante mortem
remains a challenge for the clinician.9,13 This
difficulty has multiple origins which include
the undefined aetiology, often mild and non-
specific clinical signs, poor sensitivity and
specificity of most of the imaging or clinico-
pathological findings, frequent concomitant
disorders and difficulty in obtaining or inter-
preting biopsy samples.
Little is known about the aetiology of pancre-
Aetiology – what do we know?
atitis in cats. Experimental studies, when cats
were used as a model for human disease,
revealed that total or partial obstruction of the
pancreatic duct was associated with develop-
ment of chronic changes in the pancreas.14,15
Though naturally occurring AP associated
with obstruction of the pancreatic duct, either
 R E V I E W / Pancreatitis in cats – what’s the clinical significance?

by an intraluminal mass, pancreatolith or clinical sign commonly observed in cats with

cholelith blocking the common duct near the IBD or cholangitis, may raise the intraluminal
sphincter of Oddi or by extraluminal com- pressure and further increase the risk of pan-
In the
pression, has occasionally been described in creaticobiliary reflux.4 It is also possible that
clinical cases,16–18 this does not appear to be a all three organs may be affected by a similar
majority of
common cause of pancreatic inflammation in immune-mediated disease process, such as
feline patients,
cats.3,7 occurs in some human diseases.22,23
Several studies have shown a strong associ- This concept of triaditis, and particularly
despite
ation between pancreatitis, inflammatory the association between cholangitis and pan-
bowel disease (IBD) and cholangitis in cats, creatitis, has recently been challenged.24 While
thorough

and the association of concomitant inflamma- accepting that triaditis was probably common
investigations,
tory diseases in the liver, pancreas and intes- in a subset of cats with severe liver disease,
tine has given rise to the term ‘triaditis’.7,19,20 particularly those with neutrophilic cholangi-
no obvious
The pathogenesis underlying this association tis, it has been suggested that cholangitis is
is not clear but may be explained partially by otherwise rarely associated with pancreatitis
cause of

the common insertion of the common bile and IBD.24 The strong association between
pancreatitis is
duct and the major pancreatic duct into the chronic pancreatitis and IBD was not contest-
duodenal papilla.4 It is theorised that this ed, however.24
diagnosed and
close anatomical proximity may favour reflux the disease is Ischaemia is another recognised cause of
of bile or luminal contents, including bacteria, acute pancreatitis in cats.25 This is particularly
into the pancreatic ducts. When feline pan- significant during surgery when inadvertent
considered to
creases affected by acute or chronic pancreati- compression or ligature of the pancreatic
tis were evaluated by fluorescence in situ vessels can compromise pancreatic blood
be idiopathic.
hybridisation, bacteria were detected in 35% flow.1 Similarly, hypotensive episodes during
of the organs, mainly in periductal areas or anaesthesia can induce ischaemic insults to the
glandular parenchyma.21 Streptococcus species pancreas. This seems to be an uncommon post-
and Escherichia coli were most frequently operative complication when the principles of
found, which supports the suspicion of appropriate surgical technique and careful
enteric bacterial translocation. Vomiting, a anaesthetic monitoring are respected.26,27

Clinical signs – what should we be looking for?

Mild cases of pancreatitis, particularly in patients with chronic dis- pain and gastrointestinal signs predominate.
ease, are believed to remain subclinical or to be associated with The most common signs remain highly non-specific: anorexia
mild clinical signs that go undetected by the owners.6,13 In one in 63–97% of cases and lethargy in 28–100%.4,7,8,12 On physical
study, 45% of healthy cats showed evidence of pancreatic lesions examination, weight loss, dehydration, pallor or icterus are
on post-mortem examination.6 Most of the studies evaluating frequently noted.4,7,8,12 Fever is not a common feature of feline
clinical signs of pancreatitis in cats were performed before the pancreatitis, unlike in canine patients; only 25% of feline patients
development of sensitive pancreatic are presented with hyperthermia,
tests and improvement in imaging tech- whereas hypothermia is noted in
niques. Patient recruitment in these almost 50% of patients.4 Occasionally,
studies was, therefore, biased towards a cranial abdominal mass can be
clinically severe cases, suggesting that palpated.7,12
the frequency of clinical signs is proba- Interestingly, although the signs
bly overestimated. associated with CP are believed to be
In contrast to their canine counter- milder than the signs referable to
parts, cats with pancreatitis rarely AP,6,13 a study of 63 cats with pancre-
display specific clinical signs. Gastro - atitis failed to show any difference in
intestinal signs, such as vomiting, clinical presentation between the two
diarrhoea or abdominal pain, are forms of the disease.8 This again
frequently absent or are not observed stresses the mild nature of clinical
by owners; cats present a particular signs in cats with acute disease, com-
problem in this regard, tending as a pared with dogs.
species to ‘hide’ abdominal pain.4,7,8,12 Taken together, the low frequency
Vomiting has been reported in 35–61% of gastrointestinal signs and higher
of cases (Figure 3), with diarrhoea frequency of non-specific systemic
(11–33%) and abdominal pain (19%) signs probably markedly influence the
reported less frequently.4,7,8,12 This is propensity of the clinician to suspect
in contrast to the clinical picture pancreatitis and request the appropri-
observed in dogs, where abdominal Figure 3 Frequently nausea is not obvious in cats, but ate investigations
can be associated with hypersalivation or anorexia

Downloaded from jfm.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 2, 2014 JFMS CLINICAL PRACTICE 397
R E V I E W / Pancreatitis in cats – what’s the clinical significance?

Pancreatic ischaemia is also a consequence of

pancreatitis itself. Inflammation, oedema or
fibrosis can increase pancreatic interstitial and
The clinical value of specific pancreatic function
ductal pressure and lead to compromised
tests is more variable in cats than in humans
pancreatic blood flow and further pancreatic
inflammation.28,29 This vicious cycle helps to
or dogs.
explain how CP can become progressive.
Other rare proposed aetiologies for feline and amylase activities have classically been
pancreatitis include specific infectious agents considered to be of limited value in cats, being
(Toxoplasma gondii, feline herpesvirus 1, feline extremely insensitive and showing non-specif-
infectious peritonitis virus, calicivirus, pan- ic increases associated with liver, renal or other
creatic and liver flukes), organophosphate gastrointestinal diseases.2,3,7,12,13 However,
poisoning, lipodystrophy, acute hypercal- moderate to good sensitivity and specificity of
caemia, idiosyncratic drug reactions and lipase has been reported for the diagnosis of
nutritional causes.3,4,6,30 feline pancreatitis using the 1,2-o-dilauryl-rac-
In the majority of feline patients, despite glycero-3-glutaric acid-(6’-methylresorufin)
thorough investigations, no obvious cause of ester (or DGGR-lipase) catalytic assay, when
pancreatitis is diagnosed and the disease is compared with histology as the gold
considered to be idiopathic.3,7,9 This may standard.31 A cut-off value of 26 IU/l had a
partly explain the relatively low degree of sensitivity of 100% for diagnosing AP but only
clinical suspicion that exists for feline pancre- 48% for CP, and a specificity of 63%. This test
atitis in many cases. had a high agreement with the value of Spec
fPL, and sensitivity and specificity of Spec fPL
were not significantly different from the sensi-
tivity and specificity of DGGR-lipase.32
Laboratory findings – are there any

Normocytic, normochromic, regenerative or Serum feline trypsin-like immunoreactivity

specific clinicopathological markers?

non-regenerative anaemia is a frequent observa- (fTLI) is a species-specific immunoassay that

tion in cats with AP, occurring in 26–55% of has been developed to assess pancreatic func-
cases, although it may only become apparent tion in cats. However, a range of studies have
after correction of dehydration.4,7,8 Leukocytosis reported a relatively low sensitivity of the
is less commonly noted than in dogs, seen in assay for the diagnosis of feline pancreati-
around 46% of cases.4,7,8 Leukopenia can be tis.13,33–35 In one study, the sensitivity of fTLI
observed and may be associated with a poorer was increased to 86% when the cut-off was
prognosis.4 Haematological findings were not decreased from 100 µg/l to 49 µg/l, although
significantly different between CP and AP and this probably also reduced the specificity,
between AP and acute suppurative pancreatitis which was not calculated in the study.34
in two studies in cats, and remain non-specific.7,8 A species-specific immunoassay to detect
Biochemistry changes are frequently pancreatic lipase (feline pancreatic lipase
observed but may reflect the presence of con- immunoreactivity or fPLI) has been devel-
current disease and, again, are not specific for oped in the hope that this will be more useful
pancreatitis. High activities of alanine amino- than lipase, amylase or fTLI.36 There are cur-
transferase (24–68%) and alkaline phos- rently two different tests commercially avail-
phatase (50%) have been described.4,7,8 able for the measurement of fPLI, both from
Elevation of liver enzyme activity was more the same laboratory: Spec fPL and Snap fPL
pronounced in cats with CP than AP in one (Idexx). Both tests are a monoclonal sandwich
study, suggesting this may represent the effect enzyme-linked immunosorbent assay
of concomitant hepatobiliary inflammatory (ELISA). Spec fPL is a quantitative test, for
disease.8 Hyperglycaemia is a common abnor- which concentrations >5.3 µg/l are consistent
mality (10–64%) and is observed in both AP with pancreatitis and concentrations between
and CP; hypoglycaemia is more frequently 3.5 and 5.3 µg/l are in a grey zone. Snap fPL,
found in cats with AP.4,7,8 Ionised hypo - now available in veterinary practices, is a
calcaemia has been reported particularly semi-quantitative test. A positive Snap fPL
frequently in cats with AP (32–61% of cases), test result indicates a fPLI value >3.5 µg/l and
and was associated with a poorer outcome in does not differentiate patients in the grey zone
several studies.4,7,8,31 Hypokalaemia was also from patients with values of fPLI considered
commonly found in one study, affecting 56% consistent with pancreatitis. A positive Snap
of patients.7 As with haematology, biochem- fPL result must, therefore, be further con-
istry results do not appear to be significantly firmed by a Spec fPL assay.
different between patients with CP and AP . There is still a paucity of studies evaluating
The clinical value of specific pancreatic func- the value of Spec fPL in the diagnosis of feline
tion tests is more variable in cats than in other pancreatitis.32,35,37 In the only clinical study in
species, including humans and dogs. Lipase which the diagnosis of pancreatitis was based

398 JFMS CLINICAL PRACTICEDownloaded from jfm.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 2, 2014

on histopathology, fPLI appears to be the most
sensitive test, compared with fTLI or comput-
ed tomography (CT), with a sensitivity of
100% for moderate or severe pancreatitis.35
The sensitivity was much lower for mild pan-
creatitis, at 54%, with an overall sensitivity for
all cases (mild, moderate and severe) of 67%,
which was still higher than other tests.35
However, histopathology was only performed
when deemed possible by the clinician, intro-
ducing some bias in the recruitment of
patients. In the same study, specificity when
evaluating eight healthy cats was 100%.35 The
number of healthy cats was low in this study
and when three cats with a normal pancreas
but signs consistent with pancreatitis were
evaluated the specificity dropped to 67%.35
Obviously, more studies with higher num-
bers of healthy cats, or cats with other gastro-
intestinal diseases, are needed to properly
evaluate the sensitivity and specificity of fPLI,
but it does appear to be one of the most sensi-
tive and specific blood tests for feline pancre-
atitis currently available. All these diagnostic
values relate to Spec fPL. To date, Snap fPL
has not been validated by independent stud-
ies, although validation studies have been
performed by the manufacturer. Moreover,
lesions such as fibrosis or atrophy are not
expected to induce increases in fPLI levels.37
This would suggest that the sensitivity of fPLI
in diagnosing CP without an active compo-
nent is low, and may explain the lower sensi-
tivity for mild pancreatitis.35,37
Despite, therefore, being the most powerful
non-invasive test for the diagnosis of feline
pancreatitis that is currently available, it is
important to remember that fPLI is not 100%
sensitive and specific, especially for mild
and/or chronic forms of pancreatitis, and that
more studies are needed to strengthen the
evaluation of its efficacy.38
Figure 4 Ultrasonographic findings in a cat with acute pancreatitis. Note the
heterogeneous pancreatic parenchyma and surrounding hyperechoic
mesentery (arrows). Courtesy of diagnostic imaging department, Queen’s Veterinary
School Hospital, University of Cambridge, UK
Downloaded from jfm.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 2, 2014
R E V I E W / Pancreatitis in cats – what’s the clinical significance?
Abdominal radiographs may reveal a cranial
Imaging – is it any help?
loss of serosal detail and/or a mass effect.
However, radiography is both insensitive and
non-specific for the diagnosis of feline pancre-
atitis and is mainly recommended to rule out
concomitant diseases such as intestinal
obstruction.7,8,13,34
Ultrasonographic findings that suggest AP
in dogs, such as a hypoechoic pancreas,
hyperechoic mesentery and abdominal effu-
sion, are also relatively specific for pancreati-
tis in cats (Figure 4), although other pancreatic
lesions (eg, neoplasia, hyperplastic nodules)
may share a similar appearance with pancre-
atitis.35,39 Ultrasound findings are relatively
specific in differentiating pancreatitis from
other gastrointestinal diseases, but ultrasound
lacks specificity to differentiate between AP
and CP; indeed, there is considerable overlap
in ultrasound findings between the two forms
of the disease.8 It is important to recognise
Some changes that some changes detected during abdominal
ultrasonography may be age related, like pan-
creatic duct dilation, previously thought to be
detected during
a specific sign for pancreatitis (Figure 5).39
In cats, abdominal ultrasound carries a low
abdominal
sensitivity (11–35%) for pancreatitis,8,33,34,40
ultrasonography
although one study reported a 67% sensitivity
in moderate to severe pancreatitis, with a
may be age
lower sensitivity in the mildest forms of
disease.35 The sensitivity of abdominal
related, like
ultrasound is further influenced by difficulties
pancreatic duct
in detecting the pancreas in some patients,
and is dependent on operator experience.33,40
dilation,
The use of endosonography (endoscopic
ultrasound) may improve general visualisa-
previously
tion of the feline pancreas, but in one study
thought to be
did not alter the diagnosis of pancreatitis
when compared with transcutaneous abdom-
a specific sign
of pancreatitis. inal ultrasound despite improving general
visualisation.41
Figure 5 Dilation of the pancreatic duct can be a normal finding in ageing
cats. Courtesy of diagnostic imaging department, Queen’s Veterinary School
Hospital, University of Cambridge, UK
JFMS CLINICAL PRACTICE 399
R E V I E W / Pancreatitis in cats – what’s the clinical significance?

Despite the above-mentioned limitations, Multiple biopsies are,

abdominal ultrasonography is recommended therefore, recommend-
in any suspected case of feline pancreatitis, as it ed to reach a definitive
may be useful to diagnose associated pancreat- diagnosis and pancre-
ic masses (eg, pseudocysts, tumours or abscess- atitis cannot be com-
es), and pancreatic or biliary stones, and will pletely excluded on the
allow fine-needle aspiration of lesions.12,40 basis of a negative biop-
The use of CT in the diagnosis of feline sy result.4,38
pancreatitis has been evaluated in two Lesions observed
clinical studies,34,35 which revealed a similarly during CP are frequent-
low sensitivity of 20%. CT is thus not ly mild in severity and
recommended as a diagnostic aid for feline it is suspected that
pancreatitis.34,35 Magnetic resonance cholan- histopathology may be
giopancreatography (MRCP) is becoming the relatively insensitive
imaging modality of choice in humans for the for diagnosing mild
pancreatic and biliary tract, and a recent study lesions.6 Conversely,
in cats suggested that magnetic resonance mild forms of CP were
imaging and MRCP may also be helpful in frequently found in
cats with pancreatitis.42 asymptomatic patients
in one study.6 The find-
ing of mild signs of
The gold standard for ante-mortem diagnosis inflammation on pan-
Histology – an ideal gold standard?

of pancreatitis in cats remains histopatholo- creatic biopsy can be a diagnostic challenge,

gical analysis of pancreatic biopsies,3,6,8,35 therefore, as these lesions may represent
Figure 6 Intraoperative view
of a cat with severe acute

despite most authors agreeing that histo- ongoing pancreatitis but may not necessarily
pancreatitis. Note the

pathology is not perfect for evaluating the explain the patient’s clinical signs.
areas of haemorrhagic
parenchyma, and overall

presence of feline pancreatitis. Pancreatic Until recently there was no detailed descrip-
swollen and oedematous

biopsy is often complicated by the sensitivity tion of the histological assessment of feline
appearance of the pancreas.

of the pancreas to hypoxaemia, whether pancreatitis. The above-mentioned study has

Courtesy of Jane Ladlow,
Queen’s Veterinary School

induced by hypotension during anaesthesia proposed criteria for diagnosing AP and CP

Hospital, University of

or by pancreatic blood flow impairment fol- histologically and for scoring the severity of
Cambridge, UK

lowing manipulations of other organs during lesions.6 This represents the first histological
surgery. Moreover, most cats with severe pan- classification of natural feline clinical pancre-
creatitis are poor candidates for anaesthe- atitis. However, previous studies have been
sia.4,38 Even for patients stable enough to characterised by a marked variation in the
undergo anaesthesia and pancreatic biopsy, or description of the lesions and the severity of
improving on supportive treatment, pancreat- AP and CP, making histology less than ideal
ic biopsy may not be recommended as the as a gold standard.
results rarely alter patient management in
these cases.
Pancreatic biopsy should be considered if
laparotomy or laparoscopy are being per-
Pancreatic biopsy is not considered to increase
formed for other reasons.38 The trauma
induced by performing pancreatic biopsy is
the risk of pancreatitis provided it is performed

not, in itself, considered to increase the risk of

carefully and there is no disruption to the
pancreatitis, so clinicians should not be reluc-
tant to collect pancreatic biopsies at laparoto-
pancreatic blood supply.
my provided they are careful and do not
disrupt the blood supply. Gross lesions associ-
ated with AP include oedema, hyperaemic or
haemorrhagic parenchyma (Figure 6) and
Conclusions on why feline pancreatitis is so overlooked

signs of focal peritonitis. CP is usually associ-

The prevalence of histological lesions consistent with pancreatitis is high

ated with fewer changes, although severe

in feline patients.6 Despite this, pancreatitis is uncommonly suspected

areas of fibrotic tissue and adhesions to the

clinically in cats due to infrequent and non-specific clinical signs.

small intestine may be observed.

Studies also show that achieving a diagnosis is challenging because most

Histological accuracy is limited by frequent

of the tests have limited sensitivity and specificity, particularly in relation

multifocal distribution of lesions in cats with

to chronic and/or mild forms of the disease. The challenges are

AP or CP.6,7,40 In a study comparing the pres-

compounded by the limitations of histology, the gold standard test for

ence of pancreatitis lesions in the left limb, the

the diagnosis of feline pancreatitis. To diagnose feline pancreatitis the

right limb and the body of the pancreas, only

clinician must then integrate the results of multiple tests to improve

half of the cats diagnosed with pancreatitis

sensitivity and specificity. All this would suggest that numerous cases of

had lesions identified in every section.6

feline pancreatitis will remain undiagnosed, although it also possible that
some mild pancreatic changes have limited clinical significance.

400 JFMS CLINICAL PRACTICEDownloaded from jfm.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 2, 2014
 R E V I E W / Pancreatitis in cats – what’s the clinical significance?

was not associated with response to insulin in

one study.46 It is recommended that clinicians
What is the clinical significance

look for pancreatitis when investigating

of feline pancreatitis? It is
The significance of the clinical signs in acutely insulin resistance in a diabetic cat.
recommended
and severely ill feline patients diagnosed with End-stage CP with loss of acinar tissue is
pancreatitis cannot be denied.3,4,7,8,12,38 Some of believed to be the main cause of exocrine pan-
to look for
these cats will present with severe clinical syn- creatic insufficiency (EPI) in cats.3,4,9,48 At the
dromes like cardiovascular shock, disseminat- time of diagnosis of EPI, pancreatic histology
pancreatitis

ed intravascular coagulation, pulmonary predominantly shows fibrosis with loss of

thromboembolism and multi-organ failure.3,38
But these severe presentations are rare and the
investigating
most frequent type of feline pancreatitis diag-
nosed in practice is a mild form of CP. Given
the high numbers of asymptomatic cats with
resistance in
histological evidence of mild pancreatitis,6 the
clinical significance of finding mild pancreati-
a diabetic cat.
tis on histological sections has to be ques-
tioned. It is possible that mild pancreatitis is
not pathological in some patients, or may rep-
resent a response of the pancreas to concur-
rent disease.
However, there is now growing evidence
that pancreatitis can be associated with other
concurrent diseases, such as cholangitis and
IBD, as discussed earlier. Hepatic lipidosis has
also frequently been associated with feline
pancreatitis.8,43,44 This is not surprising consid-
ering that anorexia and weight loss are a typi-
cal feature of feline pancreatitis. The reported
prevalence of pancreatitis lesions in cats
with hepatic lipidosis varies from study to
study from 5–38%.43,44 In one study compar-
ing AP and CP, concomitant hepatic lipidosis
was found to be more frequent in association
with CP (30% prevalence) than AP (9%).8
These values, based on retrospective studies,
when
pancreatic acinar tissue and minimal inflam-
mation (the pancreatic equivalent of a cirrhot-
insulin ic liver).48 In one case series of 16 cats with
EPI, no cat was clinically suspected of pancre-
atitis prior to diagnosis of EPI. Pancreatic
histopathology was performed in two cats,
with findings reported as ‘pancreatic atro-
phy’, although the authors did not
clarify whether this was associated with
extensive fibrosis typical of end-stage CP.49
In this case series, EPI was diagnosed on the
basis of low serum fTLI in all the cats in which
it was measured, together with compatible
clinical signs (weight loss and diarrhoea).
Serum cobalamin was low in all the cats test-
ed,49 which is to be expected in EPI in this
species because cats make all of their intrinsic
factor required for ileal absorption of
cobalamin in their pancreas. It is, therefore,
important to consider a possible diagnosis of
EPI in a cat with unexplained weight loss,
with or without concurrent DM, and consider
measuring both fTLI and cobalamin in these
cases.
Treatment recommendations

likely underestimate the true prevalence of Most of the recommendations for the treatment
the association between feline pancreatitis of feline pancreatitis are based on extrapola-
and hepatic lipidosis. It is worth noting, too, tions from human studies or experimentally
that the presence of AP is considered a poor induced feline pancreatitis. Evidence is, there-
prognostic factor in a patient with hepatic lipi- fore, lacking and prospective studies evaluat-
dosis.43 ing the effect of different aspects of treatmen-
The high frequency of pancreatitis in feline ton on spontaneous disease are needed.
patients with diabetes mellitus (DM) has been The general recommendations are centred
emphasised in several studies.8,12,45,46 There is on three main aspects of management: nutri-
likely to be a complex cause-and-effect rela- tion and antiemetic treatment, correction of
tionship between DM and pancreatitis in cats, fluid and electrolyte imbalances, and analge-
as there is in dogs and humans. DM can pre- sia.3,4,9,37
dispose to pancreatitis; conversely end-stage
CP can lead to the development of DM by loss
of islet cells, and these cases may additionally It has long been recommended that food is
Nutrition and antiemesis

develop concurrent exocrine deficiency.45 A withheld for 24–48 h in patients with pancre-
study investigating the prevalence of pancre- atitis, but this dogma has recently been chal-
atitis in cats with DM found that fPLI was lenged in both human and canine patients.50–52
Hepatic
commonly elevated, suggesting that acute Vomiting is not a common feature in cats,
lipidosis has
episodes of pancreatic inflammation were rel- which are often presented with a history of
atively frequent in diabetic cats.46 Feline pan- anorexia of several days’ duration and com-
frequently been
creatitis is also commonly found in cats with monly show evidence of concomitant hepatic
diabetic ketoacidosis, and some authors have lipidosis. Starvation can, therefore, be detri-
associated

suggested that pancreatitis may play a role in mental in feline patients, and it is now accept-
with feline
the development of ketoacidosis by decreas- ed that feeding should be instigated as soon as
ing sensitivity to insulin,45,47 although fPLI possible.4,53
pancreatitis.

Downloaded from jfm.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 2, 2014 JFMS CLINICAL PRACTICE 401
R E V I E W / Pancreatitis in cats – what’s the clinical significance?

Table 1 Drugs used to treat pancreatitis in cats

Drug Dose Licensed Comments

for use in
cats (UK)
Buprenorphine 0.005–0.03 mg/kg IV, SC, IM, Yes Can produce sedation and, rarely, respiratory
PO depression
Butorphanol 0.1–0.5 mg/kg IV, SC, IM
0.1–0.2 mg/kg/h CRI
Yes Reduced efficacy in cats compared with
dogs
Antiemetics
0.5–1.0 mg/kg PO
are indicated
Analgesics

Methadone 0.1–0.2 mg/kg SC, IM q6–8h No Can produce dysphoria

Morphine 0.1–0.4 mg/kg IV, SC, IM No Can cause dysphoria, respiratory depression in all cats with
0.1 mg/kg/h CRI and nausea
suspected
Fentanyl 25 mg/h patch, with half No Effect will start 6 h and last 4 days after
patches exposed application pancreatitis,
Tramadol 2–4 mg/kg PO q8–12h No No pharmacokinetic studies performed in
cats. Dysphoria possible whether or
Ketamine 2 µg/kg min CRI Yes Used concomitantly with lidocaine and/or
morphine CRI. Dysphoria possible
not vomiting
Lidocaine 0.1 mg/kg/h CRI No Risk of lidocaine toxicity is present, as
Metoclopramide 0.2–0.4 mg/kg IV, SC, IM, PO Yes Can induce neurological toxicity. May have a nausea can
Antiemetics

1–2 mg/kg/day CRI negative effect on the sphincter of Oddi

Maropitant 1 mg/kg SC q24h Yes be hard to
Ondansetron 0.1–1.0 mg/kg slow IV q12–24h No
recognise.
Dolasetron 0.5–1.0 mg/kg IV, PO q24h No
Cimetidine 5–10 mg/kg q8h No Can induce confusion if overdosed
Antacids

Ranitidine 1–2 mg/kg q8–12h No Mild prokinetic effect. Risk of hypotension

when injected rapidly IV
Famotidine 0.5 mg/kg IV, SC, IM No Risk of hypotension when injected rapidly IV.
0.5–1.1 mg/kg PO Potential risk of intravascular haemolysis
Omeprazole 0.7 mg/kg q24h PO, IV No Can decrease intestinal absorption of other
drugs (eg, cobalamin)
Sucralfate 0.25–0.5 g q8h PO No Can decrease intestinal absorption of other
Others

drugs
Cobalamin 150–500 µg SC once weekly for Yes
6 weeks, then every 1–2 months
IV = intravenously, SC = subcutaneously, IM = intramuscularly, PO = orally, CRI = constant rate infusion

There is currently no evidence that a low fat
diet is beneficial in cats with pancreatitis. Due
to the peculiarities of feline metabolism, it is
generally suggested that affected cats are fed a
diet that is low in carbohydrate, high in pro-
tein and contains a moderate amount of fat in
sion, and may be more useful in cases that
have functional ileus due to its prokinetic
effects.54 It may interfere with splanchnic per-
fusion via its dopamine antagonist action and
with sphincter of Oddi activity via its choliner-
gic effect, although the significance of these
Figure 7 Gastrostomy

order to avoid the development of malnutri- effects has not been investigated clinically.55,56
feeding tubes allow

tion and hepatic lipidosis.9,53 Nutrition should Nausea is more reliably controlled in
administration of
appropriate volumes of food

be reintroduced gradually over a few days to cats with pancreati-

and can be used for

avoid refeeding syndrome.53 tis by NK-1 receptor

medication administration

It is extremely important to recognise and antagonist (maropi-

treat nausea in cats, as it can severely reduce tant) or 5HT3 antag-
food intake.4,54 Signs of nausea in cats include onist (ondansetron,
vomiting or hypersalivation (see Figure 3), but dolasetron) agents.54
can also be poorly specific; anorexia, for There is also evi-
example, may be the only reported sign. dence that maropi-
Anti-nausea medications (Table 1) are there- tant has a beneficial
fore indicated in all cats with suspected pan- effect in reducing
creatitis, whether or not vomiting is present. visceral pain in cats,
Metoclopramide is considered to be poorly which further sup-
effective in the feline species but may be more ports its use in feline
effective when given as a constant rate infu- pancreatitis.57

402 JFMS CLINICAL PRACTICEDownloaded from jfm.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 2, 2014
 R E V I E W / Pancreatitis in cats – what’s the clinical significance?

If voluntary food intake is not restored

rapidly, it may be necessary to place a feeding
tube to allow energy requirements to be met.
Table 2 Examples of commercially available convalescence

Naso-oesophageal, oesophagostomy and gas-

veterinary diets that can be used with a feeding tube

trostomy tubes (Figure 7) are used most

Diet Calories Proteins Fat Carbo- Comments

frequently in patients with AP.53 Use of a

(kcal/ (% DM) (% hydrates

gastrojejunostomy tube, placed either surgi-

100 g DM) DM) (% DM)

cally or endoscopically, has also been

Hill’s a/d 467 44 30 16 More liquid when warmed.

described.58 It is unclear if bypassing the

Canine/Feline Can be diluted with water

pancreas is beneficial in cats. Pre-pyloric

Critical Care and blended

feeding has been shown to be safe in humans

Royal Canin 478 42 25 19 A sachet of 50 g can be

and dogs, and may also be in cats. In the acute

Convalescence diluted with water for a
Support Feline total volume of 200 ml

stages of pancreatitis, the cat may be too

unstable to have a general anaesthetic for
Royal Canin 465 49 26 6 One volume of the diet
Recovery can be diluted with one

placement of a feeding tube, particularly if

volume of water

there is concurrent hepatic lipidosis. In these

Purina 458 47 33 5 One volume of the diet

circumstances, placement of a naso-

Convalescence can be diluted with one

oesophageal feeding tube for a few days will

CN volume of water

allow stabilisation prior to placement of a

Abbott Animal 442 36 22 29 Liquid form, which is well

more secure tube.

Health CliniCare suited to naso-

Convalescence liquid veterinary diets can

Canine/Feline oesophageal tube feeding.

be used with naso-oesophageal tubes, while a

Liquid Diet Not available in the UK

semi-solid diet should be reserved for larger

DM = dry matter

tubes (oesophagostomy and gastrostomy

tubes) (Table 2). Convalescence diets are
energy-dense and have a high protein content,

Additional treatments to consider

Cobalamin injection
Vitamin B12 deficiency is common in cats with chronic
gastrointestinal disease.63 Cats with end-stage CP may also
have a deficiency due to lack of pancreatic intrinsic factor.
If blood sampling reveals low cobalamin, vitamin B12 should
be supplemented parenterally.
Antacids
H2 antagonists (cimetidine, ranitidine, famotidine) may
be useful in some patients. Ranitidine also has prokinetic
effects on the gastrointestinal tract, which may be beneficial
in cases of functional ileus secondary to pancreatitis.

Pancreatic enzyme supplements

Antibiotics
Some studies in human patients with CP have found that
Based on the higher risk of colonisation of the pancreas
pancreatic enzyme replacement therapy has been
by colonic bacteria in patients with pancreatitis compared
associated with decreased frequency and severity of painful
with healthy patients, and the relatively high frequency of
episodes of pancreatic disease, despite apparent normal
pancreatic infection in cats with AP and CP,21,64 some
exocrine pancreatic function.66 To date, no studies have
authors recommend using broad-spectrum antibiotics
been performed to confirm this effect in veterinary patients,
when severe AP is suspected.4 However, the use of
but the authors have occasionally treated cats with CP with
prophylactic antibiotics is controversial. In humans,
enzymes and found anecdotal evidence of improvement
there is no evidence that prophylactic antibiosis reduces
of gastrointestinal signs and anorexia. Certainly, any cat
infectious complications in AP, so it is not used routinely.65
with EPI as a result of end-stage CP should receive
There is no evidence in cats to demonstrate or refute
enzyme supplementation.
whether antibiotics improve outcome.

Surgery
Surgical management of feline pancreatitis is not recommended in mild to moderate cases, but should
be considered in cats with persistent biliary or pancreatic duct obstruction (particularly with choleliths),
neoplasia, severe necrosis or pancreatic abscess.4,67 In humans, any surgery on the pancreas or biliary
tract is delayed for a month after an acute flare-up of pancreatitis, unless there is a suspicion of neoplasia
in which case the intervention is rapid.65 Again, there is no good evidence in cats to guide the choice and
timing of surgical intervention.

Downloaded from jfm.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 2, 2014 JFMS CLINICAL PRACTICE 403
R E V I E W / Pancreatitis in cats – what’s the clinical significance?

which makes them appropriate for hospi-

talised feline pancreatitis patients, despite
their high fat content. In the case of severe
KEY POINTS
malnutrition and persistent anorexia, total or < Pancreatitis in cats is increasingly recognised by veterinarians,
partial parenteral nutrition may be consid-
ered, although studies in humans support
but remains frequently overlooked.
< In cats, AP is less prevalent than CP but the two presentations
combining this with at least some enteral
nutrition, where possible, to maintain gut wall
share similar clinical signs and diagnostic findings.

barrier function.53,59
< Despite increased awareness of the disease, suspecting and
confirming feline pancreatitis is a challenge in the clinical setting.

Vomiting, anorexia and diarrhoea can lead to

Lack of sensitivity or specificity of the available diagnostic tools,
Correction of electrolyte imbalances

severe dehydration and electrolyte imbal-

especially for CP, and the frequency of asymptomatic disease

ances in cats with pancreatitis.3,4 Aggressive

have led to the false idea that pancreatitis may not be clinically

intravenous fluid therapy is required to avoid

relevant.
< In the light of its association with other diseases, including
the further deleterious effects of decreased
pancreatic perfusion. Hypokalaemia and
hepatic lipidosis, cholangitis, IBD, diabetes mellitus and EPI,

hypocalcaemia are not uncommon and must

it is important that clinicians maintain a high index of suspicion

be treated, as their presence is associated with

for pancreatitis, and investigate accordingly.

a poorer prognosis.4,31

Pain is a common feature of feline pancreatitis

Analgesia

but is classically difficult to evaluate in this

species.60 Opioids are the recommended In cases of intractable pain, fentanyl injec-
first-line drugs for treating abdominal pain tion or patches, or ketamine and lidocaine
associated with pancreatitis.3,60 Morphine has constant rate infusions can be considered.60
been associated with increased sphincter of For management of chronic pain, sublingual
Oddi activity and its use in AP has previously buprenorphine or tramadol can be safe,
been questioned. However, recent human meta- although potentially less potent, alterna-
analysis failed to show increased adverse effects tives.60,62
when treating human pancreatitis patients with
opioids, while the need for supplementary
analgesia was decreased, supporting their use Other treatments that may be considered for
Other treatments

for the management of pancreatitis.61 cats with pancreatitis, in addition to the above
Buprenorphine, butorphanol and methadone mainstay treatments, are discussed on page
are the drugs most often used (see Table 1). 403.

In: Washabau RJ and Day MJ (eds). Canine and

feline gastroenterology. 1st ed. St Louis: Saunders
Funding

The authors received no specific grant from any Elsevier, 2013, pp 821–848.
funding agency in the public, commercial or not-for- 5 Bradley EL. A clinically based classification
profit sectors for the preparation of this article. system for acute pancreatitis. Summary of the
International Symposium on Acute Pancreatitis,
Atlanta, Ga, September 11 through 13, 1992.
Arch Surg 1993; 128: 586–590.
Conflict of interest

The authors do not have any potential conflicts of 6 De Cock HEV, Forman MA, Farver TB and Marks
interest to declare. SL. Prevalence and histopathologic characteris-
tics of pancreatitis in cats. Vet Pathol 2007; 44:
39–49.
7 Hill RC and Van Winkle TJ. Acute necrotizing
References

1 Owens JM, Drazner FH and Gilbertson SR. pancreatitis and acute suppurative pancreatitis
Pancreatic disease in the cat. J Am Anim Hosp in the cat, a retrospective study of 40 cases
Assoc 1975; 11: 83–89. (1976–1989). J Vet Intern Med 1993; 7: 25–33.
2 Duffell SJ. Some aspects of pancreatic disease in 8 Ferreri JA, Hardam E, Kimmel SE, Saunders HM,
the cat. J Small Anim Pract 1975; 16: 365–374. Van Winkle TJ, Drobatz KJ, et al. Clinical differen-
3 Williams DA. The pancreas. In: Guilford WG, tiation of acute necrotizing from chronic non-
Center SA, Strombeck DR, Williams DA and Meyer suppurative pancreatitis in cats: 63 cases
DJ. Strombeck’s small animal gastroenterology. 3rd (1996–2001). J Am Vet Med Assoc 2003; 223: 469–474.
ed. Philadelphia: Saunders, 1996, pp 381–410. 9 Williams DA. Feline exocrine pancreatic disease.
4 Washabau RJ. Necrosis and inflammation: feline. In: Bonagura JD and Twedt DC (eds). Kirk’s

404 JFMS CLINICAL PRACTICE Downloaded from jfm.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 2, 2014
 R E V I E W / Pancreatitis in cats – what’s the clinical significance?

current veterinary therapy. Vol XIV. St Louis: Maastricht, Netherlands. Amsterdam.

Saunders Elsevier, 2009, pp 538–543. 25 Glenn TM and Lefer AM. Role of lysosomes in the
10 Mansfield CS and Jones BR. Review of feline pan- pathogenesis of splanchnic ischemia shock in
creatitis part one: the normal feline pancreas, the cats. Circ Res 1970; 27: 783–797.
pathophysiology, classification, prevalence and 26 Smith AL, Wilson AP, Hardie RJ, Krick EL and
aetiologies of pancreatitis. J Feline Med Surg 2001; Schmiedt CW. Perioperative complications after
3: 117–124. full-thickness gastrointestinal surgery in cats
11 Xenoulis PG, Suchodolski JS and Steiner JM. with alimentary lymphoma. Vet Surg 2011; 40:
Chronic pancreatitis in dogs and cats. Compend 849–852.
Contin Educ Pract Vet 2008; 30: 166–181. 27 Mehler SJ. Complications of the extrahepatic bil-
12 Simpson KW, Shiroma JT, Biller DS, Wicks J, iary surgery in companion animals. Vet Clin North
Johnson SE, Dimski D, et al. Ante mortem diagno- Am Small Anim Pract 2011; 41: 949–967.
sis of pancreatitis in four cats. J Small Anim Pract 28 Reber HA, Karanjia ND, Alvarez C, Widdison AL,
1994; 35: 93–99. Leung FW, Ashley SW, et al. Pancreatic blood flow
13 Steiner JM. Diagnosis of pancreatitis. Vet Clin in cats with chronic pancreatitis. Gastroenterology
North Am Small Anim Pract 2003; 33: 1181–1195. 1992; 103: 652–659.
14 Karanjia ND, Singh SM, Widdison AL, Lutrin FJ 29 Patel AG, Reber PU, Toyama MT, Ashley SW and
and Reber HA. Pancreatic ductal and interstitial Reber HA. Effect of pancreaticojejunostomy on
pressures in cats with chronic pancreatitis. Dig fibrosis, pancreatic blood flow, and interstitial
Dis Sci 1992; 37: 268–273. pH in chronic pancreatitis. A feline model. Ann
15 Zhao P, Tu J, Martens A, Ponette E, Van Surg 1999; 230: 672–679.
Steenbergen W, Oord JV and Fevery J. Radiologic 30 Bayliss DB, Steiner JM, Sucholdolski JS, Radecki
investigations and pathologic results of experi- SV, Brewer MM, Morris AK, et al. Serum feline
mental chronic pancreatitis in cats. Acad Radiol pancreatic lipase immunoreactivity concentra-
1998; 5: 850–856. tion and seroprevalences of antibodies against
16 Steiner JM and Williams DA. Feline exocrine pan- Toxoplasma gondii and Bartonella species in
creatic disorders. Vet Clin North Am Small Anim client-owned cats. J Feline Med Surg 2009; 11:
Pract 1999; 29: 551–575. 663–667.
17 Bailiff NL, Norris CR, Seguin B, Griffey SM and 31 Kimmel SE, Washabau RJ and Drobatz KJ.
Ling GV. Pancreatolithiasis and pancreatic Incidence and prognostic value of low plasma
pseudobladder associated with pancreatitis in a ionized calcium concentration in cats with acute
cat. J Am Anim Hosp Assoc 2004; 40: 69–74. pancreatitis: 46 cases (1996–1998). J Am Vet Med
18 Mayhew PD, Holt DE, McLear RC and Washabau Assoc 2001; 219: 1105–1109.
RJ. Pathogenesis and outcome of extrahepatic bil- 32 Oppliger S, Hartnack S, Riond B, Reusch CE and
iary obstruction in cats. J Small Anim Pract 2002; Kook PH. Agreement of the serum Spec fPLTM
43: 247–253. and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6’-
19 Weiss DJ, Gagne JM and Armstrong PJ. methylresorufin) ester lipase assay for the deter-
Relationship between inflammatory hepatic dis- mination of serum lipase in cats with suspicion
ease and inflammatory bowel disease, pancreati- of pancreatitis. J Vet Intern Med 2013; 27:
tis, and nephritis in cats. J Am Vet Med Assoc 1996; 1077–1082.
209: 1114–1116. 33 Swift NC, Marks SL, MacLachlan NJ and Norris
20 Callahan Clark JE, Haddad JL, Brown DC, Morgan CR. Evaluation of serum feline trypsin-like
MJ, Van Winkle TJ and Rondeau MP. Feline immunoreactivity for the diagnosis of pancreati-
cholangitis: a necropsy study of 44 cats tis in cats. J Am Vet Med Assoc 2000; 217: 37–42.
(1986–2008). J Feline Med Surg 2011; 13: 570–576. 34 Gerhardt A, Steiner JM, Williams DA, Kramer S,
21 Simpson KW, Twedt DC, McDonough SP, Craven Fuchs C, Janthur M, et al. Comparison of the sen-
M, Steffey M and Dudak JL. Culture-independent sitivity of different diagnostic tests for pancreati-
detection of bacteria in feline pancreatitis. In: tis in cats. J Vet Intern Med 2001; 15: 329–333.
21st ACVIM Forum, Denver, Colorado, June 15–18, 35 Forman MA, Marks SL, De Cock HEV, Hergesell
2011. EJ, Wisner ER, Baker TW, et al. Evaluation of
22 Weismüller TJ, Wedemeyer J, Kubicka S, serum feline pancreatic lipase immunoreactivity
Strassburg CP and Manns MP. The challenges in and helical computed tomography versus con-
primary sclerosing cholangitis – aetiopathogene- ventional testing for the diagnosis of feline
sis, autoimmunity, management and malignancy. pancreatitis. J Vet Intern Med 2004; 18: 807–815.
J Hepatol 2008; 48: S38 –S57. 36 Steiner JM, Wilson BG and Williams DA.
23 Bateman AC and Deheragoda MG. IgG4-related Development and analytical validation of a
systemic sclerosing disease – an emerging and radioimmunoassay for the measurement of feline
under-diagnosed condition. Histopathology 2009; pancreatic lipase immunoreactivity in serum.
55: 373–383. Can J Vet Res 2004; 68: 309–314.
24 Williams DA. Feline triaditis: a critical review of 37 Xenoulis PG and Steiner JM. Canine and feline
the literature and new insights. Proceedings of pancreatic lipase immunoreactivity. Vet Clin Path
the 22nd ECVIM-CA Congress; Sept 6–8, 2012; 2012; 41: 312–324.

Downloaded from jfm.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 2, 2014 JFMS CLINICAL PRACTICE 405
R E V I E W / Pancreatitis in cats – what’s the clinical significance?

38 Armstrong PJ and Williams DA. Pancreatitis in JS, Robertson ID and Hosgood G. A pilot study to
cats. Top Companion Anim Med 2012; 27: 140–147. assess tolerability of early enteral nutrition via
39 Hecht S, Penninck DG, Mahony OM, King R and esophagostomy tube feeding in dogs with severe
Rand WM. Relationship of pancreatic duct dila- acute pancreatitis. J Vet Intern Med 2011; 25:
tion to age and clinical findings in cats. Vet Radiol 419–425.
Ultrasound 2006; 47: 287–294. 54 Trepanier L. Acute vomiting in cats: rational treat-
40 Saunders HM, VanWinkle TJ, Drobatz K, Kimmel ment selection. J Feline Med Surg 2010; 12: 225–230.
SE and Washabau RJ. Ultrasonographic findings 55 Dobi I and Kekesi V. Factors influencing the vas-
in cats with clinical, gross pathologic and histo- cular action of dopamine in the canine mesen-
logic evidence of acute pancreatic necrosis: 20 teric bed. Acta Chir Hung 1989; 30: 251–260.
cases (1994–2001). J Am Vet Med Assoc 2002; 221: 56 Coelho JC, Moody FG, Senninger N and Li YF.
1724–1730. Effects of gastrointestinal hormones on Oddi’s
41 Schweigheuser A, Gaschen F, Steiner JM, sphincter and duodenal myoelectric activity and
Allenspach K, Francey T and Gashen L. pancreatobiliary pressure. Studies in the opos-
Evaluation of endosonography as a new diagnos- sum. Arch Surg 1985; 120: 1060–1604.
tic tool for feline pancreatitis. J Feline Med Surg 57 Niyom S, Boscan P, Twedt DC, Monnet E and
2009; 11: 492–498. Eickhoff JC. Effect of maropitant, a neurokinin-1
42 Marolf AJ, Kraft SL, Dunphy TR and Twedt DC. receptor antagonist, on the minimum alveolar
Magnetic resonance (MR) imaging and MR concentration of sevoflurane during stimulation
cholangiopancreatography findings in cats with of the ovarian ligament in cats. Vet Anaesth Analg
cholangitis and pancreatitis. J Feline Med Surg 2013; 40: 425–431.
2013; 15: 285–294. 58 Jennings M, Center SA, Barr SC and Brandes D.
43 Akol KG, Washabau RJ, Saunders HM and Successful treatment of feline pancreatitis using
Hendrick MJ. Acute pancreatitis in cats with an endoscopically placed gastrojejunostomy
hepatic lipidosis. J Vet Intern Med 1993; 7: 205–209. tube. J Am Anim Hosp Assoc 2001; 37: 145–152.
44 Center SA, Crawford MA, Guida L, Erb HN and 59 Chan DL, Freeman LM, Labato MA and Rush JE.
King J. A retrospective study of 77 cats with Retrospective evaluation of partial parenteral
severe hepatic lipidosis. J Vet Intern Med 1993; 7: nutrition in dogs and cats. J Vet Intern Med 2002;
349–359. 16: 440–445.
45 Goossens MMC, Nelson RW, Feldman EC and 60 Robertson SA. Managing pain in feline patients.
Griffey SM. Response to insulin treatment and Vet Clin North Am Small Anim Pract 2008; 38:
survival in 104 cats with diabetes mellitus 1267–1290.
(1985–1995). J Vet Intern Med 1998; 12: 1–6. 61 Basurto Ona X, Rigau Comas D and Urrútia G.
46 Forcada Y, German AJ, Noble PJM, Steiner JM, Opioids for acute pancreatitis pain. Cochrane
Suchodolski JS, Graham P, et al. Determination of Database Syst Rev 2013 Jul 26; 7: CD009179.
serum fPLI concentrations in cats with diabetes DOI: 10.1002/14651858.CD009179.pub2.
mellitus. J Feline Med Surg 2008; 10: 480–487. 62 Giordano T, Steagall PV, Ferreira TH, Minto BW, de
47 Bruskiewicz KA, Nelson RW, Feldman EC and Sá Lorena SE, Brondani J, et al. Postoperative
Griffey SM. Diabetic ketosis and ketoacidosis in analgesic effects of intravenous, intramuscular,
cats: 42 cases (1980–1995). J Am Vet Med Assoc 1997; subcutaneous or oral transmucosal buprenor-
211: 188–192. phine administered to cats undergoing ovario-
48 Steiner JM and Williams DA. Serum feline hysterectomy. Vet Anaesth Analg 2010; 37: 357–366.
trypsin-like immunoreactivity in cats with 63 Simpson KW, Fyfe J, Cornetta A, Sachs A, Strauss-
exocrine pancreatic insufficiency. J Vet Intern Med Ayali D, Lamb SV, et al. Subnormal concentra-
2000; 14: 627–629. tions of serum cobalamin (vitamin B12) in cats
49 Thompson KA, Parnell NK, Hohenhaus AE, with gastrointestinal disease. J Vet Intern Med
Moore GE and Rondeau MP. Feline exocrine 2001; 15: 26–32.
pancreatic insufficiency: 16 cases (1992–2007). 64 Widdison AL, Karanjia ND and Reber HA. Routes
J Feline Med Surg 2009; 11: 935–940. of spread of pathogens into the pancreas in a
50 Qin HL, Su ZD, Hu LG, Ding ZX and Lin QT. feline model of acute pancreatitis. Gut 1994; 35:
Effect of early intrajejunal nutrition on pancreat- 1306–1310.
ic pathological features and gut barrier function 65 Tenner S, Baillie J, DeWitt J and Vege SS. American
in dogs with acute pancreatitis. Clin Nutr 2002; 21: College of Gastroenterology guideline: manage-
469–473. ment of acute pancreatitis. Am J Gastroenterol 2013;
51 McClave SA, Chang WK, Dhaliwal R and Heyland 108: 1400–1416.
DK. Nutrition support in acute pancreatitis: a sys- 66 Puylaert M, Kapural L, Van Zundert J, Peek D,
tematic review of the literature. J Parenter Enteral Lataster A, Mekhail N, et al. Pain in chronic pan-
Nutr 2006; 30: 143–156. creatitis. Pain Pract 2011; 11: 492–505.
52 Chan DL. The inappetent hospitalised cat: clini- 67 Son TT, Thompson L, Serrano S and Seshadri R.
cal approach to maximising nutritional support. Surgical intervention in the management of
J Feline Med Surg 2009; 11: 925–933. severe acute pancreatitis in cats: 8 cases
53 Mansfield CS, James FE, Steiner JM, Suchodolski (2003–2007). J Vet Emerg Crit Care 2010; 20: 426–435.

406 Available online at jfms.com

Reprints and permission: sagepub.co.uk/journalsPermissions.nav
JFMS CLINICAL PRACTICE Downloaded from jfm.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 2, 2014