Topics in Compan An Med 27 (2012) 133-139

Topical Review

Chronic Pancreatitis in Dogs

Penny Watson, MA, VetMD, CertVR, DSAM, DipECVIM, MRCVS

A B S T R A C T

Keywords:
chronic pancreatitis
exocrine pancreatic insufficiency
diabetes mellitus
IgG4⫹ sclerosing disease
English Cocker Spaniel
ultrasound
pancreatic histology
Department of Veterinary Medicine, Univer-
sity of Cambridge, Cambridge, United King-
dom
Address reprint requests to: Penny Watson,
MA, VetMD, CertVR, DSAM, DipECVIM,
MRCVS, Department of Veterinary Medicine,
University of Cambridge, Madingley Road,
Cambridge CB3 OES, United Kingdom.
Chronic pancreatitis used to be considered uncommon in dogs, but recent pathological and clinical studies
have confirmed that it is in fact a common and clinically significant disease. Clinical signs can vary from
low-grade recurrent gastrointestinal signs to acute exacerbations that are indistinguishable from classical
acute pancreatitis. Chronic pancreatitis is a significant cause of chronic pain in dogs, which must not be
underestimated. It also results in progressive impairment of endocrine and exocrine function and the
eventual development of diabetes mellitus or exocrine pancreatic insufficiency or both in some affected
dogs at end stage. The etiology is unknown in most cases. Chronic pancreatitis shows an increased
prevalence in certain breeds, and recent work in English Cocker Spaniels suggests it is part of a
polysystemic immune-mediated disease in this breed. The histological and clinical appearance is different
in different breeds, suggesting that etiologies may also be different. Diagnosis is challenging because the
sensitivities of the available noninvasive tests are relatively low. However, with an increased index of
suspicion, clinicians will recognize more cases that will allow them to institute supportive treatment to
improve the quality of life of the patient.

E-mail: pjw36@cam.ac.uk. 䉷 2012 Elsevier Inc. All rights reserved.

Chronic pancreatitis (CP) is a re-emerging disease in dogs. Until re-
cently, acute pancreatitis was believed to be much commoner than
chronic disease in this species. However, recent pathology studies
have revealed a very high prevalence of CP in dogs, with strong breed
predispositions. The resultant increased clinical suspicion is increas-
ing its diagnosis in living animals, confirming its clinical importance.
Recognition of this disease is important because its acute and chronic
sequelae can have significant effects on the quality of life of the dog
and, as long as they are recognized, can often be treated effectively.
Definition of Chronic Pancreatitis
There has been some confusion in the veterinary literature over
the definition of acute and chronic pancreatitis. It is important to
define these diseases accurately to allow studies on the etiology and
treatment, which may not be the same in acute and chronic disease.
As in other organs of the body (acute vs. chronic renal failure or acute
vs. chronic hepatitis), the definition should be histological and func-
tional. CP is defined as a continuing inflammatory disease of the pan-
creas characterized by irreversible morphological changes that typi-
cally cause pain and/or permanent loss of function.1,2 Histologically, it
is associated with fibrosis, gradual loss of pancreatic tissue, and a
mononuclear inflammatory cell infiltrate (lymphocytic or lymphop-
lasmacytic) (Fig. 1). It is distinguished from acute pancreatitis not by
temporal factors (length of clinical signs) but predominantly by re-
versibility of histological changes in the pancreas. Acute disease is
typified by necrosis, edema, and a neutrophilic infiltrate. In acute dis-
ease, provided the patient recovers, the pancreas returns to normal
both histologically and functionally, whereas in CP, there is perma-
nent histological change and progressive loss of exocrine and endo-
crine function,1 which may progress to exocrine pancreatic insuffi-
ciency (EPI) and/or diabetes mellitus (DM) if the dog lives long
enough.3,4 The pancreas has an enormous functional reserve capacity,
so these diseases only develop if more than 80% to 90% of functional
mass is lost.5,6 Therefore, many dogs will not reach end stage by the
end of their lives.
The confusion in the veterinary literature usually occurs due to
defining the disease as acute if it presents acutely or has any acute
inflammatory infiltrate on histology: so an acute flare-up of chronic
disease is often termed “acute pancreatitis.” CP often results in acute
flare-ups because fibrosis in the pancreas reduces its distensibility
and results in duct blockage during secretion. This largely explains
why CP is progressive. On histology, an acute-on-chronic pancreatitis
results in a mixed inflammatory infiltrate with neutrophils, edema,
and necrosis admixed with lymphocytes and underlying fibrosis. Rec-
ognizing that there is in fact underlying chronic disease is very impor-
tant in these cases because it increases the index of suspicion for
reduction in function and the development of chronic sequelae and
recurrent disease, which increases the likelihood of the clinician rec-
ognizing and treating these sequelae (see below).
Many dogs do not in fact have a pancreatic biopsy, so the diagnosis
of “acute” or “chronic” pancreatitis remains clinical in many cases.
This inevitably leads to confusion: it is possible to have recurrent
acute pancreatitis, which mimics ongoing chronic disease, and it is not
uncommon for both humans and dogs with CP to present initially as a
clinically severe, apparently isolated acute bout of pancreatitis after a
long subclinical phase of low-grade disease has already destroyed
much of the pancreatic parenchyma.1,4,7 Even more confusingly, some
(but by no means all) cases of CP start as recurrent, acute disease.1,7 In
fact, the relationship between recurrent acute and chronic pancreati-
tis is a controversial one in human medicine and the subject of ongo-
ing debate.1,8 It is now generally accepted that some cases of human
CP represent a progression from acute disease (such as occurs in alco-
holic and hereditary disease), whereas others may begin as chronic
disease (such as autoimmune CP) and some cases remain acute and
never become chronic (such as pancreatitis associated with gall
stones).9,10 The concept of a disease beginning as chronic may sound
odd, but if the definition is histological rather than temporal (as pro-

0958-3947/$ – see front matter 䉷 2012 Topics in Companion Animal Medicine. Published by Elsevier Inc.
http://dx.doi.org/10.1053/j.tcam.2012.04.006
134 Penny Watson / Topics in Companion An Med 27 (2012) 133-139

posed in CP), then this is possible in the sense that the inflammatory Table 1
infiltrate is mononuclear from the beginning of the disease. The link Breeds showing increased risk of chronic pancreatitis in the United Kingdom2,4

between acute and chronic disease in dogs has never been specifically ● Cavalier King Charles Spaniels
investigated, but it is very likely that, as in humans, some cases begin ● English Cocker Spaniels
● Boxers
as chronic disease (such as the disease in English Cocker Spaniels
● Collies
[ECS] described below), whereas other chronic cases develop from
recurrent acute disease. A variety of other breeds and also cross-breeds have also been reported with chronic
The clinician may not suspect underlying chronic disease until it pancreatitis.
reaches end stage and the dog develops EPI or DM. This may explain
why the true prevalence of canine CP was unrecognized for many
years. However, studies both in humans and dogs show that up to 40% and pancreatic histology, whereas only 5 out of 63 dogs had solely
of acute pancreatitis cases are actually acute-on-chronic histologi- acute disease.12
cally.11 A recent study in dogs found histological evidence of concur-
rent acute and chronic changes in 58 out of 63 dogs with pancreatitis Prevalence and Breed Relationships

Recent pathological and clinical studies have identified distinctive

breed prevalences for canine CP, at least in the United Kingdom. A
study of postmortem samples from predominantly old dogs found an
overall prevalence of CP of between 25% and 34%, depending on
whether autolyzed cases were included or excluded from the analy-
sis2 A number of breeds, particularly spaniels, appeared to be over-
represented in both this and a clinical study.2,4 Breeds predisposed to
CP are listed in Table 1. ECSs appear to present commonly with mul-
tisystemic disease, as described below, with CP forming only part of
the syndrome—and not always the most clinically obvious part (Fig.
2). Cavalier King Charles Spaniels (CKCS) appear to show less obvious
clinical signs and diagnostic imaging findings than other breeds, sug-
gesting their disease is less inflammatory. Boxer dogs are predisposed
to CP but appear to be resistant to the development of end-stage

Fig. 1. Histology of pancreas in dogs with chronic pancreatitis. (A) Section of

pancreas from a Collie with mild chronic pancreatitis. There is a focal area of
lymphocytic inflammation (dark cells) with early surrounding fibrosis (red staining)
(Sirius red stain. Bar ⫽ 50 ␮m). (B) Section of pancreas taken postmortem from an old
wire-haired Fox Terrier, which presented to a charity clinic for investigation of
polydipsia and polyuria. Diabetes mellitus was confirmed on investigations and the
owner declined treatment, so the dog was euthanized. The dog was in poor body
condition with a dry coat, and a serum trypsin-like immunoreactivity measured
before death confirmed that the dog also had exocrine pancreatic insufficiency. The
pancreas was not grossly visible at postmortem, but there were areas of fibrosis and
adhesions adjacent to the proximal duodenum. Sections of this area showed the
changes visible in this section—large areas of fibrosis (stained light pink on the slide) Fig. 2. English Cocker Spaniels, like this dog, are predisposed to chronic pancreatitis
with only a few remaining islands of acinar tissue (stained darker pink on this slide) in the United Kingdom. They often have immune-mediated disease in other organs,
and no visible islets. A histological and clinical diagnosis of end-stage chronic including keratoconjunctivitis sicca, as seen in this dog. This dog is being restrained
pancreatitis was made (hematoxylin and eosin stain; bar ⫽ 50 ␮m). gently for abdominal ultrasound.
 Penny Watson / Topics in Companion An Med 27 (2012) 133-139
Table 2
Typical clinical signs in dogs with chronic pancreatitis (in approximate order of
frequency) that would increase index of suspicion of disease and encourage further
investigations
1. Low-grade waxing and waning gastrointestinal signs (intermittent anorexia
with or without vomiting or diarrhea). The typical pattern is anorexia first,
followed by vomiting and then diarrhea (often colitis-like features because of
proximity of left pancreatic limb and transverse colon) 24 hours later.
2. Occasional anorexia and frequent evidence of postprandial pain and learned
food aversions, without other gastrointestinal signs (often only recognized by
the owner in hindsight when the dog is given analgesia and the signs resolve).
3. Acute presentation with signs typical of acute pancreatitis as a single episode or
recurrent acute flare-ups, often after a long period of subclinical disease or of
mild clinical signs 1 and 2 above.
4. Diabetes mellitus developing in an older dog of a predisposed breed (see Table
1) particularly if combined with a history of recurrent gastrointestinal signs.
5. Exocrine pancreatic insufficiency in an older dog of a breed other than German
Shepherd Dog.
6. Concurrent diabetes mellitus and exocrine pancreatic insufficiency in any dog.
7. Sudden onset of extrahepatic biliary obstruction.
8. Back pain (when all other causes such as intervertebral disk disease have been
ruled out) and polydipsia/polyuria have also been reported.
9. Keratoconjunctivitis sicca or protein-losing nephropathy in an English Cocker
Spaniel increases the index of suspicion for a generalized disease also involving
the pancreas (see text).
disease (EPI and DM), suggesting a very good regenerative response in
their pancreas.13 Dogs diagnosed with CP are typically middle-aged to
older at diagnosis,4 although the disease tends to be well advanced by
the time of diagnosis so the age at onset of the disease is unknown in
either humans or dogs. Similar prevalence studies have not been un-
dertaken in the United States, but anecdotally, reports to the author
from North American dog owners and veterinarians suggest that sim-
ilar breeds may be affected on both sides of the Atlantic.
Pathogenesis and Etiology
There are many potential etiologies of CP in humans, which have
been summarized using the TIGAR-O system.1 This divides the causes
of CP into Toxic-metabolic (such as smoking-related and alcoholic),
Idiopathic, Genetic, Autoimmune, Recurrent and severe acute pancre-
atitis, and Obstructive. In industrialized nations, long-term alcohol
misuse accounts for 50% to 90% of cases of CP depending on the study
and country14 although genetic predispositions to alcoholic CP also
exist because only about 10% of heavy drinkers have clinically recog-
nized pancreatitis.1 These genetic predispositions to environmental
triggers are usually complex and polygenic and are gradually being
unraveled in humans. It is likely that similar interactions between
genes and environment occur in dogs. For example, high-fat foods
trigger pancreatitis in some dogs but not others, and perhaps fat is to
dogs what alcohol is to humans. Genetic studies in dogs remain very
sparse. Studies in miniature Schnauzers have shown variations in the
SPINK1 gene (serine protease inhibitor Kazal type 1, which is another
name for pancreatic secretory trypsin inhibitor).15 Mutations in this
gene in humans are not sufficient alone to cause spontaneous pancre-
atitis but are recognized to increase susceptibility to alcoholic pancre-
atitis,14 so perhaps these variations in miniature Schnauzers also in-
crease susceptibility to environmental triggers. Much more work will
be necessary in dogs to confirm this.
It has been suggested in both human medicine and veterinary
medicine that the pattern of fibrosis on histology might reflect the
underlying cause.16,17 ECSs have a histologically distinctive disease
characterized by perilobular progressive fibrosis and duct destruc-
tion. Affected dogs often develop concurrent keratoconjunctivitis
sicca, glomerulonephritis, and other immune-mediated diseases, sug-
gesting similarities to human autoimmune pancreatitis17 (Fig. 2). As
described in the human disease, ECS showed periductal fibrosis, a
T-cell– dominated lymphocytic infiltrate and duct destruction. A re-
135
cent immunohistochemical study has demonstrated that the ECS
disease is strongly associated with an infiltration of plasma cells se-
creting one subclass of IgG (IgG4), which is associated with glomeru-
lonephritis as well as pancreatitis in affected dogs.18 This is remark-
ably similar to the human disease that is now reclassified as IgG4⫹
sclerosing disease to stress the polysystemic nature of the disease19
Human autoimmune pancreatitis is now divided into 2 types: type 1,
which is IgG4⫹ and multisystemic, affecting the kidney, liver, tear
ducts, and other organs as well as the pancreas, and type 2 autoim-
mune disease, which is confined to the pancreas and gut.20
What about the etiology in other breeds of dog with CP? The cause
remains unknown in other breeds, but histological differences in dif-
ferent breeds are highly suggestive of different etiologies.2,17 Some
dogs such as Terriers and Collies show intra-acinar lesions suggestive
of premature enzyme release, whereas Boxers show a dense lym-
phoplasmacytic periductular infiltrate, which might suggest autoim-
mune disease, but without obvious duct destruction or polysystemic
disease. CKCSs show a predominance of periductular and perivascular
fibrosis and ductular hyperplasia. More work is indicated to investi-
gate the etiology in all these breeds.
Presenting Clinical Signs
Dogs with CP most commonly present with intermittent, low-grade gas-
trointestinal signs, although some may present acutely with acute pancre-
atitis, extrahepatic biliary obstruction, or even acute diabetic ketoacidotic
crisis without any previous suspicion of underlying chronic disease.4 Devel-
opment of EPI in an older dog that is not of a breed predisposed to pancreatic
acinar atrophy (i.e., not a German Shepherd Dog) has to increase the index of
suspicion of underlying CP. Other potential clinical signs that should prompt
investigation of potential CP are listed in Table 2.
Potential Acute and Chronic Sequelae of Disease and Contribution to
Diabetes Mellitus and Exocrine Pancreatic Insufficiency in Dogs
Potential acute and chronic sequelae of CP in dogs are listed in
Table 3. End-stage CP results in the development of either DM or EPI or
both if the dog lives long enough to lose 80% to 90% of pancreatic mass
before death. Whether DM or EPI develop first seems to vary between
individual dogs, but exocrine and endocrine function appear to dete-
riorate approximately in parallel21 and often insufficiencies of each
will develop within 6 to 12 months of each other.3,4
End-stage CP is almost certainly a more important contributor to
the etiology of DM in dogs than currently recognized. CP is being
increasingly recognized as a significant cause of other specific types of
DM (type 3c) in humans.22 The available veterinary literature strongly
supports an association between DM and pancreatitis (both acute and
chronic) in dogs in both naturally occurring and experimental pancre-
atitis, and suggests that approximately 30% of cases of canine DM may
be caused by end-stage CP.3,4,23,24 There is a complex cause-and-effect
Table 3
Potential acute and chronic sequelae of chronic pancreatitis in dogs
1. Acute flare-up: potentially life-threatening episode of acute-on-chronic pan-
creatitis
2. Development of pancreatic pseudocyst or abscess
3. Extrahepatic biliary obstruction (usually reversible as inflammation subsides
and surgery usually unnecessary)
4. Diabetes mellitus
5. Exocrine pancreatic insufficiency with or without cobalamin deficiency because
of lack of pancreatic intrinsic factor. Subsequent development of cachexia if
exocrine pancreatic insufficiency is not recognized and treated.
6. Possible pancreatic adenocarcinoma (circumstantial evidence only in dogs—
known association with chronic pancreatitis in humans). Note: Beware of erro-
neous diagnosis of neoplasia in a dog with an inflammatory mass on imaging.
English Cocker Spaniels particularly can present with these mass-like lesions as
reported in human IgG4⫹ sclerosing disease (see text and Fig. 3).
136 Penny Watson / Topics in Companion An Med 27 (2012) 133-139
relationship between DM and pancreatitis in dogs: in some cases,
preexisting DM of another cause seems to predispose to acute pan-
creatitis,11,25 whereas in other cases, DM appears to be the result of
islet loss in end-stage CP3,4 (Fig. 1B). The cause-and-effect relationship
between pancreatitis and DM can therefore be difficult to ascertain in
clinical cases without pancreatic histology. The author would have a
high index of suspicion that DM in any older dog of a breed predis-
posed to CP such as Cocker Spaniel or CKCS may in fact be caused by
CP. Awareness of the potential relationship in high-risk breeds is im-
portant to increase the index of suspicion of concurrent EPI which
otherwise might be unrecognized and untreated.
The association between EPI and end-stage CP is incontrovertible.
However, clinicians often fail to recognize that EPI can result from end-
stage CP in dogs because of the high prevalence of pancreatic acinar
atrophy (PAA) in young German Shepherd Dogs as a cause of EPI. The
failure to recognize the gradual onset of EPI in an older dog with CP can
be disastrous because the dog may become progressively more and more
cachexic and ultimately be euthanized for what should be a treatable
complication of CP3 if recognized and appropriately treated. PAA is cur-
rently believed to be the commonest cause of EPI in dogs and CP is re-
ported to be an uncommon cause.26 This is in contrast to humans and
cats in which end-stage CP is the commonest cause of EPI and PAA is not
recognized.1,27 In the 1960s and 1970s, CP was reported to be a common
disease in dogs and a common cause of EPI in this species. In the first
volume of Ettinger’s Textbook of Veterinary Internal Medicine in 1975, the
authors of the chapter on pancreatic disease,28 often referencing another
published review of canine pancreatitis,29 noted that, using histology as
the gold standard, CP was the most common canine pancreatic disease
and that it was a common cause of EPI in this species. They noted that DM
was also often seen in CP in association with pancreatic insufficiency,
particularly in older dogs. Therefore, recognizing CP as a common disease
in the 21st century, predisposing to the development of DM and EPI in
older dogs, is as so often in veterinary medicine not a novel finding, but a
rediscovery of a forgotten disease.
Diagnosis of concurrent EPI and DM in a dog should greatly in-
crease the suspicion of underlying CP as the cause of both diseases.
The occurrence of DM or EPI in an older ECS or CKCS greatly increases
the index of suspicion for underlying CP.
Diagnosis
Diagnosis of CP can be very challenging because of the nonspecific
and often low-grade nature of the clinical signs and the relatively low
sensitivity of noninvasive diagnostic tests. This is also recognized in
human medicine where, even with sophisticated imaging techniques,
there is a suspected high level of underdiagnosis. There are in fact 2
challenges to the diagnosis of CP in dogs: (1) to differentiate it from
other potential diseases causing similar clinical signs; and (2) to de-
termine whether the dog has acute pancreatitis (either a single bout
or recurrent acute disease) or chronic disease.
The latter is not very important for immediate treatment deci-
sions, which are symptomatic and depend on the severity of the dis-
ease at presentation (see section on treatment below). However, rec-
Table 4
Sensitivity of diagnostic tests for diagnosis of chronic pancreatitis in 14 dogs with histologically confirmed disease (from Watson et al 20104)
Trypsin-like Canine Pancreatic Lipase
Immunoreactivity Immunoreactivity in Gray
⬎ 35 ng/mL Range or Higher
Sensitivity for diagnosis of 17 (10-49) 58 (34-79)
CP % (and 95%
confidence interval)
95% confidence intervals are very wide because of the small numbers of dogs.
* 102-200 ng/mL (gray range) or ⬎ 200 ng/mL (diagnostic of pancreatitis). Note: 3⫻ reference range was used because of the published known background activity of these
enzymes. Values of both enzymes just above the reference range have a higher sensitivity but likely a very low specificity (see Watson et al 20104).
ognizing the potential for chronic underlying disease and functional
impairment is very important for long-term treatment.
The clinician has to maintain a high index of suspicion and con-
sider ruling out CP in any case with the clinical signs described above
and in Table 2 at either the acute or chronic end of the spectrum. The
differential diagnoses for the low-grade clinical signs are other causes
of intermittent gastrointestinal signs, including chronic inflammatory
bowel disease and renal and hepatic disease. The differential diagno-
ses for acute exacerbations are other causes of an acute abdomen. In
addition, the common concurrent occurrence of diseases in other or-
gans, either related to the CP or coincidental in an old dog, can confuse
and complicate diagnosis.
The gold standard for diagnosis of CP is pancreatic histology.1,2
However this is rarely performed antemortem in either humans or
dogs because it is invasive, with a risk of significant morbidity and
does not usually alter treatment decisions. It can therefore not be
ethically justified unless the dog is having a laparotomy for another
reason. If that is the case, the veterinary clinician should not be afraid
to take a (careful) pancreatic biopsy of the tip of a lobe together with
biopsies of other organs as part of their investigations. In the author’s
experience, the risk of significant postoperative pancreatitis is very
low as long as the surgeon is gentle and does not obstruct the pancre-
atic blood supply. This impression was supported by a recent study of
the effects of pancreatic biopsy with clamshell forceps in normal dogs,
which showed only mild histological and serum enzyme changes af-
ter the procedure.30 A full description of the techniques for pancreatic
biopsy is beyond the scope of this article and the reader is referred to
surgical texts for more detail. It is worth taking a biopsy even if the
pancreas appears grossly normal: early cases of CP can appear normal,
whereas in later stages, the pancreas becomes obviously nodular and
adhesed to the surrounding organs. However, even histology does not
have a sensitivity of 100% for the diagnosis of CP because the disease
can be patchy. The milder the disease, the more patchy the histologi-
cal changes, so it is possible to miss the disease on histology in early
and mild cases2,31 whereas more advanced cases will have more dif-
fuse disease and a biopsy from the tip of a lobe is more likely to be
diagnostic. Unfortunately, this is the case for all diagnostic tests for CP
in both humans and dogs: the milder and earlier the disease, the
harder it is to diagnose. The tendency therefore is for early disease to
be underdiagnosed and end-stage disease to be overrepresented in
clinical studies of CP.4,32
There are a number of suggested systems for noninvasive diagno-
sis of CP in humans that rely on a combination or clinicopathological
and diagnostic imaging findings.32,33 There is no published validated
system in dogs. However, as in humans, noninvasive diagnosis must
rely on a combination of diagnostic imaging (usually transcutaneous
ultrasound) and pancreatic-specific blood tests. Table 4 shows the
published sensitivity of noninvasive diagnostic tests for diagnosis of
CP in a small number of dogs with histologically confirmed disease.
Elevated serum canine pancreatic lipase immunoreactivity (cPLI) and
transcutaneous ultrasound had the highest sensitivities, but both
were ⬍60% sensitive.
Canine Pancreatic Lipase Finding Any
Immunoreactivity ⬎ 200 Amylase 3⫻ Reference Lipase 3⫻ Reference Abnormality on
ng/mL Range or More* Range or More* Ultrasound
26 (10-51) 14 (4-37) 28 (11-54) 56 (35-75)
 Penny Watson / Topics in Companion An Med 27 (2012) 133-139
Fig. 3. Pancreatic mass lesion seen on ultrasound in an English Cocker Spaniel with
chronic pancreatitis. On first examination, pancreatic neoplasia was considered a
differential diagnosis on this dog. However, the mass resolved on subsequent
ultrasound examinations and the dog did well clinically, confirming that it was an
inflammatory and not neoplastic mass. (Image provided by the Diagnostic Imaging
Department, Queen’s Veterinary School Hospital, University of Cambridge.)
Transcutaneous ultrasound is the commonest pancreatic imaging
modality used in dogs because of its easy availability. However, its low
sensitivity for the diagnosis of CP in dogs (as already also recognized
in cats) is understandable. Ultrasound relies on edema and inflamma-
tion to produce tissue interfaces, which are much more likely in acute
than chronic pancreatitis. In the absence of these, with low-grade
inflammation, tissue loss, and fibrosis, it will have low sensitivity. It is
very important also to be aware that ultrasound is not a histological
diagnosis: some cases of CP can appear as mass lesions on ultrasound,
particularly in ECS, which mimic similar findings in human autoim-
mune pancreatitis (Fig. 3). On some occasions, these mass-like lesions
may appear on ultrasound to invade the adjacent intestinal wall be-
cause of the adhesions between the pancreas and intestine. It is im-
portant to realize that these lesions may be inflammatory and not
neoplastic and that a dog should not be euthanized because of the
gross appearance of the pancreas either on ultrasound or at laparot-
omy without histological confirmation of neoplasia. In general, large
pancreatic masses are more likely to be inflammatory than neoplastic
because pancreatic adenocarcinomas are so malignant that they
would very rarely reach a large size before the dog died of metastatic
disease.
In human medicine, endoscopic ultrasound, computed tomogra-
phy (CT), or magnetic resonance cholangiopancreatography (MRCP)
are preferred imaging modalities for diagnosis of CP, although none of
these has 100% sensitivity. Endoscopic retrograde cholangiopancre-
atography (ERCP) is also used in humans but is being replaced with
the less invasive MRCP and CT. Endoscopic ultrasound, CT, and ERCP
have all been described in dogs but in very few cases, so their sensi-
tivity and specificity for the diagnosis of CP in this species are un-
known and their availability currently limited.
The use of pancreatic-specific serum enzyme tests for diagnosis
carries a particular problem in CP: loss of tissue mass. Although cPLI
has a high sensitivity for acute pancreatitis, its sensitivity for the di-
agnosis of CP is much lower, probably because of the loss of acinar
mass in these cases. It is already known that dogs with PAA have a low
serum cPLI34 and therefore it makes sense that dogs with advanced CP
and marked loss of acinar tissue mass will not show elevations in cPLI.
Likewise, the use of serum trypsin-like immunoreactivity (TLI) to di-
agnose either EPI or pancreatitis is a problem in dogs with CP. Finding
a low serum TLI has a very high sensitivity for diagnosis of EPI in dogs
with pancreatic acinar atrophy.35 However, sensitivity of a low serum
137
TLI for the diagnosis of EPI in dogs with CP is ⬍ 100%21 This is because
concurrent ongoing pancreatic inflammation can elevate TLI, whereas
loss of tissue mass reduces it, thus resulting in some cases in a normal
TLI. It is even possible for serum TLI to be transiently elevated in the
range diagnostic of pancreatitis in a dog with underlying EPI3,4 There-
fore, repeated serum tests may be necessary to diagnose both CP and
EPI in these dogs. The author recommends that serum tests for diag-
nosis of EPI are taken when the dog has shown no gastrointestinal
signs for at least a week, whereas serum samples for diagnosis of
pancreatitis should be taken within 1 to 2 days of onset of gastroin-
testinal signs (i.e., during an acute flare-up of chronic disease). Fecal
elastase tests are used in human medicine to diagnose EPI in cases of
CP and should be more sensitive and specific than serum TLI. A canine-
specific fecal elastase has been developed and validated for use in
dogs,36 but there are conflicting reports of its usefulness for the diag-
nosis of EPI in dogs37,38 and therefore more work is necessary before it
can be recommended instead of serum TLI in this species.
Treatment
In most cases of CP, where the etiology is unknown, treatment is
supportive rather than specific. The exception to this is more specific
treatment in ECSs with suspected autoimmune disease. However,
even supportive treatment can make a big difference to the quality of
life of the patient. The 3 “pillars” of treatment of CP to be considered in
all cases are:
1. Analgesia
2. Nutrition
3. Addressing functional loss (endocrine or exocrine or both)
In addition, dogs with CP can have acute exacerbations of disease,
which are indistinguishable clinically from single isolated bouts of
acute pancreatitis. These episodes should be treated symptomatically
as described in more detail in the article by Mansfield in this issue.
Analgesia and aggressive fluid therapy are very important in the acute
bouts. The author uses a modified organ-scoring system similar to
that developed by Ruaux et al.39 to guide treatment and prognostica-
tion in these more acute cases and this seems to work as well in
acute-on-chronic cases as in truly acute cases. Early institution of nu-
tritional support is particularly important in patients with underlying
CP because they are likely already suffering from some degree of un-
derlying protein-calorie malnutrition because of developing exocrine
insufficiency.
Long-term treatment of chronic cases is again symptomatic in
most cases. Analgesia is very important. The pain associated with CP is
not to be underestimated: most human patients present to their doc-
tor complaining of chronic epigastric pain, particularly postprandi-
ally. Sometimes this is so severe and intractable to analgesics that
patients have surgery to remove the pancreas to control it.40 There is
evidence that dogs with CP also have postprandial pain and that this
often improves when they are fed a low-fat diet.4 Owners often un-
derestimate the pain their dogs have until they see the change in their
dog’s behavior after altering food and/or adding analgesics—when
they report the dog “behaving like a puppy” and no longer being picky
with food or stretching after eating. Pain referred to the lumbar spine
is reported in some humans with CP and was reported in one Cocker
Spaniel with CP.17 Royal Canin gastrointestinal Low fat diet (Royal
Canin USA Inc, St Charles, MO) or Iams Veternary Formula intestinal
Formula Low Residue diet (Proctor and Gamble Pet Care; Cincinnati’
Ohio) are good choices of low-fat clinical diets, or the client could
make a low-fat homemade diet based on chicken (without the skin) or
white fish, with the help of a veterinary nutritionist. There is no good
evidence currently that adding pancreatic enzymes to the food re-
duces postprandial pain in either humans or dogs with CP, although
they are necessary when the dog develops exocrine insufficiency (see
below).
138 Penny Watson / Topics in Companion An Med 27 (2012) 133-139
If changing to a low-fat diet is not enough, analgesics should be used.
The author follows a staged approach to analgesia similar to that de-
scribed in humans. If the dog is hospitalized for an acute bout, injectable
analgesics can and should be used with opiates, lignocaine, or ketamine
all being considered either individually or in combination. When the dog
goes home, oral analgesics may be necessary. Acetaminophen is usually
chosen as the first oral drug of choice as long as the dog has no concurrent
liver disease. This should be used with caution, but it has a veterinary
license for use in dogs in the United Kingdom. The dose used is 10 mg/kg
once or twice a day in dogs. Classical nonsteroidal antiinflammatory
drugs are best avoided because of their potential to increase gastrointes-
tinal and renal side effects in animals with CP and particularly in Cocker
Spaniels with concurrent renal disease. If acetaminophen is insufficient
alone, oral butorphanol or tramadol (2-5 mg/kg up to 2 times a day) can
be used. Buprenophine patches could also be considered for short-term
home use, but the author would not use other opiate patches at home in
these animals: if they are so painful as to require them, then they should
be hospitalized for effective analgesia and frequent pain scoring. There is
evidence that some of the pain in CP in humans is neurogenic in origin41
and the author has observed lymphocytes tracking in the nerve sheaths
of affected dogs on histology, so it is worth considering the use of drugs
for neurogenic pain in refractory cases, such as gabapentin. Substance P
has also been implicated in the pain associated with CP42 so maropitant
might be tried as an analgesic as well as an anti-emetic in these cases.
Treating intractable pain with total pancreatectomy in dogs has never
been reported. Because of differences in the anatomy and blood supply of
the pancreas, surgery to remove the whole organ would be much more
challenging than it is in humans and is not recommended.
If the dog develops diabetes mellitus or EPI, these should be
treated symptomatically. Dogs with DM secondary to CP do not seem
to have a worse prognosis or poorer response to therapy than dogs
with DM of other causes.4 This may seem surprising, given that acute
flare-ups of disease should cause diabetic instability, but it may reflect
the fact that DM only develops toward the end stage of the disease
when acute flare-ups are likely to be mild. It is important also to
recognize EPI when it develops and be proactive in adding enzymes to
the food. Serum cobalamin should also be measured and supple-
mented parenterally if it is low. The author recommends proactive
enzyme supplementation in any dog with CP that begins to lose
weight, regardless of the result of serum tests, because of their limited
sensitivity to diagnosis of EPI in CP as described above. This advice is
very similar in humans and prevents the gradual, insidious develop-
ment of protein-calorie malnutrition because of a delay in diagnosis
and treatment of exocrine insufficiency. If the dog is also receiving
insulin therapy for DM, it is important to remember that insulin re-
quirement is likely to increase because of increased nutrient absorp-
tion after enzyme supplementation.
ECSs are suspected to have CP because of a polysystemic immune-
mediated disease as described above. In humans, treatment of auto-
immune CP with immunosuppressive doses of steroids results in sig-
nificant clinical and functional improvement and is now the
treatment of choice.43 No clinical trials have been reported on the use
of steroids in ECSs with CP, but their use would seem logical and has
the potential to slow down or stop disease progression in this breed.
The difficulty is knowing how long to treat them and what to monitor
to show resolution of disease. This is also a challenge in humans43 so
more work is necessary to provide answers to these questions in both
species. The positive point, however, is that this is the first time that
any specific treatment has been proposed that could alter the out-
come for any form of pancreatitis in dogs.
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