Pancreatitis in Dogs and Cats - Digestive System - Merck Veterinary Manual

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MERCK MANUAL

Veterinary Manual
PROFESSIONAL VERSION

Pancreatitis in Dogs and Cats


By Jörg M. Steiner, Med Vet, Dr Med Vet, PhD, DACVIM-SAIM, DECVIM-CA, AGAF, Texas
A&M University System

Reviewed/Revised Oct 2020 | Modified Oct 2022


Pancreatitis is an inflammatory condition that is common in dogs and cats. It can be acute or chronic
and subclinical or associated with various clinical signs. Pancreatitis is diagnosed by integrating the clinical
picture, imaging findings, and serum lipase immunoreactivity levels. Management is centered around
diagnosis and treatment of underlying causes and risk factors, supportive care, and symptomatic
care. Management of chronic pancreatitis also requires monitoring disease progression, and, if there is no
improvement, trial therapy with an immunosuppressive agent.

Etiology and Pathogenesis of Pancreatitis in Dogs and Cats

Most cases of pancreatitis in dogs and cats are idiopathic. However, several risk factors have
been identified. Miniature Schnauzers have been reported to be dramatically overrepresented in some
studies, and it has been speculated that they may have a genetic predisposition similar to that in families of
human patients with hereditary pancreatitis. Other studies have reported an increased prevalence in
Yorkshire Terriers, Cocker Spaniels, Dachshunds, Poodles, sled dogs, or other breeds.

Dietary indiscretion is believed to be a common risk factor in dogs. Also, hypertriglyceridemia, if severe (ie,
generally serum concentrations ≥500 mg/dL), is considered a risk factor for pancreatitis in dogs but not in cats.
Hyperadrenocorticism has been cited in some studies as a risk factor for pancreatitis in dogs. Severe blunt
trauma, such as can be sustained during a traffic accident or in cats with high-rise syndrome, can also
cause pancreatitis. Surgery has been considered another risk factor; however, most postsurgical cases of
pancreatitis are now believed to be due to pancreatic hypoperfusion during anesthesia. Infectious diseases
have been implicated, but the evidence for a cause and effect relationship is weak in most cases. In dogs,
pancreatitis has been reported with Babesia canis or Leishmania infection. In cats, Toxoplasma gondii,
Amphimerus pseudofelineus, and feline infectious peritonitis are considered most important.

Many drugs have been implicated in causing pancreatitis in people, but very few have been
confirmed in dogs and cats. In general, most drugs should be viewed as potential causes of pancreatitis;
cholinesterase inhibitors, calcium, potassium bromide, phenobarbital, L-asparaginase, estrogen,
salicylates, azathioprine, thiazide diuretics, and vinca alkaloids are probably the most important.
Many different insults may ultimately lead to pancreatitis through a common pathway. Secretion of
pancreatic juice decreases during the initial stages of pancreatitis. This is followed by co-
localization of zymogen granules and lysosomes, leading to activation of trypsinogen to trypsin within the
co- localized organelles. Trypsin, in turn, activates more trypsinogen and also other zymogens. Prematurely
activated digestive enzymes lead to local damage of the exocrine pancreas with pancreatic edema,
bleeding, inflammation, necrosis, and peripancreatic fat necrosis. The ensuing inflammatory process leads
to recruitment of WBCs and cytokine production. The activated enzymes, and more importantly, the
cytokines circulate in the bloodstream and lead to distant complications such as generalized inflammation,
disseminated intravascular coagulation, disseminated lipodystrophy, pancreatic encephalopathy,
hypotension, renal failure, pulmonary failure, myocarditis, or even multiorgan failure.

Clinical Findings of Pancreatitis in Dogs and Cats

In dogs with the most severe forms of pancreatitis (ie, the patients in one study all either died or were
euthanized because of the severity of their disease), anorexia (91%), vomiting (90%), weakness (79%), abdominal
pain (58%), dehydration (46%), and diarrhea (33%) have been reported as the most common clinical signs,
but it is crucial to note that these findings don't reflect the clinical signs
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Clinical signs in cats with similarly severe forms of pancreatitis are even less specific, with anorexia
(87%), lethargy (81%), dehydration (54%), weight loss (47%), hypothermia (46%), vomiting (46%), icterus (37%),
fever (19%), and abdominal pain (19%) most commonly reported.

Dogs and cats with milder forms of pancreatitis may be subclinical or may have only vague
clinical signs, such as anorexia, lethargy, or diarrhea.

The low rate of abdominal pain reported is remarkable given that >90% of human patients with pancreatitis
report abdominal pain, so it is most likely due to lack of recognition in veterinary patients.

Diagnosis of Pancreatitis in Dogs and Cats

• Integrating clinical findings, imaging findings, and results from measurement of serum
pancreatic lipase immunoreactivity

A history of dietary indiscretion combined with vomiting and abdominal pain may suggest pancreatitis in
dogs, but most cats present with nonspecific histories and clinical signs. Findings on CBCs and serum
biochemistry profiles may suggest inflammation but are nonspecific. Changes on a CBC and chemistry
profile mainly reflect systemic complications or concurrent disease and may also help to rule out other
potential differential diagnoses.
Abdominal radiographs may show decreased detail in the proximal abdominal cavity and displacement of
abdominal organs, but these findings are also nonspecific and a diagnosis based on radiographic findings
alone is unreliable. However, abdominal radiographs are valuable in animals suspected of having
pancreatitis to exclude other differential diagnoses. Abdominal ultrasonography, if stringent criteria are
applied, is fairly specific for severe forms of acute pancreatitis, but pancreatic enlargement and fluid
accumulation around the pancreas alone are not sufficient for diagnosis. A combination of pancreatic
enlargement, fluid accumulation around the pancreas, changes in echogenicity (ie, decreased
echogenicity suggesting pancreatic necrosis, increased echogenicity around the pancreas suggesting
peripancreatic fat necrosis), and/or a pancreatic mass effect are suggestive of pancreatitis.

Care should be taken not to overinterpret findings, because modern ultrasonographic equipment has a very
high resolution, and pancreatic nodular hyperplasia may lead to changes in echogenicity, falsely
suggesting the presence of pancreatitis. Also, the sensitivity of abdominal ultrasonography is
highly operator-dependent, with sensitivities as high as 35% in cats and 68% in dogs in the most
experienced
hands.

More advanced imaging techniques such as contrast-enhanced ultrasonography,


computed tomography, or magnetic resonance imaging are not yet routinely used for the
diagnosis of pancreatitis in dogs and cats, though they may hold promise for the future.

Several diagnostic markers for pancreatitis have been evaluated in dogs and cats. The clinical usefulness of
serum amylase activity is limited in dogs and cats. Serum lipase activity can be measured using various
substrates, but none of these are specific for the measurement of pancreatic lipase activity. Some studies
have suggested that DGGR and triolein may be better substrates to measure pancreatic lipase activity in
serum, whereas other studies come to different conclusions, with a high rate of false-positive results.

In contrast, the measurement of pancreatic lipase immunoreactivity (PLI) is specific for the
measurement of pancreatic lipase concentration in serum and is thus the most specific
diagnostic test for pancreatitis. It is also highly sensitive. In-clinic tests for the semiquantitative
evaluation of serum pancreatic lipase immunoreactivity (ie, SNAP CPL and SNAP fPL) are available. A
negative semiquantitative test suggests that pancreatitis is very unlikely, whereas a positive test suggests
pancreatitis. In the latter case, pancreatic lipase immunoreactivity (PLI) concentration should be
measured in a serum sample (ie, by Spec CPL and Spec fPL) and evaluated to confirm the diagnosis and to determine a
baseline concentration. This also allows the use of serum PLI concentration as a monitoring
tool for the disease. It is important to
remember, as for any disease, that no test should be used in isolation for diagnosis, and all clinical findings
should be used in conjunction to arrive at the most appropriate diagnosis.

More recently, several quantitative in-house assays for the measurement of serum PLI concentration, mainly in
dogs, have become available. These assays have either not yet been analytically validated in the primary
literature or have failed analytic validation and thus cannot be recommended for routine use at this time.

Pancreatic cytology or histopathology can also be used to definitively diagnose pancreatitis. Fine- needle
aspiration of the pancreas is safe and can show acinar cells and inflammatory cells, allowing a definitive
diagnosis of pancreatitis. However, lack of inflammatory cells does not exclude pancreatitis, because the
inflammatory infiltrate can be highly localized. Pancreatic biopsy for histopathologic evaluation may be
associated with a higher risk of pancreatitis than fine-needle aspiration (due to more aggressive pancreatic
handling and longer anesthesia). Also, even if the presence of pancreatitis seems obvious on macroscopic
examination of the pancreas, a biopsy specimen should be collected because the definitive diagnosis of
pancreatitis requires the identification of an inflammatory infiltrate during histopathology. Finally, animals
with severe pancreatitis are often poor anesthetic risks, and exploratory laparotomy or even fine-needle
aspiration may not be justified.

Treatment of Pancreatitis in Dogs and Cats

• Acute cases: identification and management of underlying causes and risk factors, supportive care,
and symptomatic care

• Chronic cases: as above, with monitoring of progression, and, if there is no improvement, trial
therapy with an immunosuppressive agent

The mainstay of therapy of severe pancreatitis is supportive care with fluid therapy, vigorous monitoring,
and early intervention to prevent systemic complications. Fluid therapy should be based on calculation of
degree of dehydration (to be replaced over 4-8 hours if there is no contraindication), maintenance, and
ongoing losses (eg, due to vomiting or diarrhea).

In those few cases in which the cause is known, specific therapy against the inciting cause may be
initiated. Antibiotics are of questionable value and should not be used routinely.

Resting the pancreas is suggested only if the animal vomits uncontrollably (ie, the animal vomits
frequently and violently despite appropriate antiemetic therapy). In fact, early nutritional support is
considered a key component of successful treatment of human patients with severe pancreatitis. Also,
enteral nutritional support is considered superior to parenteral nutrition. Animals that vomit should be treated
with an antiemetic, such as maropitant (NK1 antagonist), ondansetron, or dolasetron (HT3 antagonists), or in most
animals a combination of both. Even animals that do not actively vomit may benefit from such antiemetic
support, because they may be nauseated, leading to poor or absent appetite. Metoclopramide is not
considered effective as an antiemetic agent and should not be used in these animals.

Abdominal pain should be assumed to be present and treated until contrary evidence is available.
Intermittent meperidine, butorphanol, or buprenorphine may be used in animals with mild or
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an opioid, such as morphine, fentanyl, or methadone, or with a combination therapy of fentanyl, ketamine,
and lidocaine. Many other treatments have been investigated in dogs, cats, and people, but unfortunately
none has been shown to be useful.
Recently, a new medication for the specific treatment of acute pancreatitis, Brenda Z, an LFA-1
antagonist, has been licensed for the treatment of acute canine pancreatitis in Japan. Although initial
reports are very promising, this medication has not yet been licensed for use in either North America or
Europe.

Animals with mild forms of pancreatitis should be carefully assessed for the presence of risk factors (eg,
hypertriglyceridemia, hypercalcemia, history of medications that can cause pancreatitis) and concurrent
diseases (eg, cholangitis, hepatitis, inflammatory bowel disease, diabetes mellitus). In dogs, feeding an
ultra-low-fat diet is crucial for treatment success. In cats, a moderately fat-restricted diet is recommended.
Antiemetic drugs (see above) and appetite stimulants (ie, capromorelin in dogs, mirtazapine in cats) are helpful
for animals that may not eat due to nausea.

If animals with chronic pancreatitis do not respond to therapy, a trial with prednisone (dogs), prednisolone
(dogs and cats), or cyclosporine (dogs or cats) may be attempted. Cyclosporine is advantageous in
animals with concurrent diabetes mellitus, because it has a smaller impact on insulin resistance than
glucocorticoids.

The prognosis in mild cases of pancreatitis is good, but the prognosis in severe cases of
pancreatitis is guarded in both dogs and cats. Systemic complications such as hypothermia, acidosis,
hypocalcemia, and single- or multiple-organ failure are considered risk factors for a poor outcome. It can
be challenging to identify severe cases early during the disease process and prevent complications in
those animals.

Key Points

• A diagnosis of pancreatitis is made by integrating clinical findings, imaging findings, and


results from measurement of serum pancreatic lipase immunoreactivity.

• Management of acute pancreatitis is centered around diagnosis and treatment of


potential underlying causes and risk factors, supportive care, and symptomatic care.

For More Information

• TAMU - Pancreatitis Information

• Also see pet health content regarding pancreatitis in cats and dogs.

MERCK
Copyright © 2023 Merck & Co., Inc., Rahway, NJ, USA and its affiliates. All rights
reserved.

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