What It Takes to Manage Acute Pancreatitis

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Acute pancreatitis is a common presentation in dogs and cats. This article discusses the presentation, diagnosis and treatment of acute pancreatitis, and provides current, practical advice to optimize the outcomes.

Clinical signs

The classic clinical signs of acute pancreatitis in dogs include vomiting, diarrhoea and cranial abdominal pain. Pancreatitis is the most common cause of extrahepatic bile duct obstruction and thus some dogs present with jaundice - sometimes several days after resolution of the acute signs of pancreatitis. In cats, however, the clinical signs are subtle and less specific for pancreatitis. Most commonly, affected cats present with non-specific loss of appetite and lethargy, in America this is colloquially known as ADR (ain’t doing right).  However, some cats present with some or all of vomiting, diarrhoea, abdominal pain, cavity effusions or poorly controlled diabetes mellitus.

In both species the severity of signs varies greatly from patients with mild, transient signs to moribund patients in a critical state. There are no pathognomic clinical findings and further testing is required to confirm the diagnosis.


In most cases of acute abdominal disease the combination of abdominal imaging and serum biochemistry are the go-to diagnostic tests and cases of suspected pancreatitis are no exception.


Amylase/lipase - severe elevations in these enzymes is suggestive of pancreatitis in dogs. However, they are neither sensitive nor specific. Elevations can also be seen with gastrointestinal disease and renal compromise (including pre-renal disease). They are of almost no value in diagnosing pancreatitis in cats.

Canine pancreatic Lipase (cPL)/1,2-o-dilauryl-rac-glycero-3-glutaric acid (6’-methylresorufin) ester (DGGR) lipase - these are different types of lipase assay offered by various laboratories for dogs. These tests are more specific and sensitive than standard lipase. Clinicians using these tests should be aware of significant limitations to the positive predictive value of these tests. By this I mean that while dogs with an elevation of these parameters are likely to have some degree of pancreatic inflammation, this does not mean that pancreatitis is the reason the patient is unwell. For example, in one Australian study of dogs presenting with acute abdomen an increased cPL was associated with a 40% rate of false positives.1 It is likely that these patients, who had other causes of acute abdomen, had secondary or concurrent pancreatitis which resulted in misleading test results. This is an important finding to be aware of as it raises the potential for dogs with a surgical acute abdomen, for example an intestinal foreign body, to test positive on cPL and be mistreated as a case of pancreatitis.

Feline pancreatic lipase (fPL) - fPL has revolutionised our ability to diagnose pancreatitis in cats.  More recently, DGGR lipase has been shown to correlate well with fPL.2 Nonetheless there are challenges with interpretation of this test as well. Several studies have demonstrated that many clinically normal cats have histopathological changes suggestive of pancreatitis3 and it is unclear how these correlate with fPL/DGGR lipase.2 As such, mild increases in fPL should be interpreted with a degree of caution, and it has been suggested that a higher cut-off, for example 10 or 12 µg/l (as opposed to the listed 3.5 µg/l), may make this test more useful in diagnosing feline acute pancreatitis (Figure 1).4

Figure 1: fPL levels above 20 are a negative prognostic indicator in cats with acute pancreatitis


Abdominal radiographs - while radiologists will tell you to look for loss of serosal detail, particularly within the right cranial abdominal quadrant, this finding lacks the sensitivity or specificity to be of great clinical use. The main role of abdominal radiographs is to look for, and exclude, surgical disease prior to initiating medical therapy for suspected acute pancreatitis. Ultrasound is the first choice imaging modality but the role of radiography to rule out an intestinal foreign body remains very important in general practice when there is reduced availability of ultrasound or experienced sonographers.

Abdominal ultrasound - where good ultrasound equipment and experienced operators are available abdominal ultrasound is the diagnostic modality of choice for acute pancreatitis in dogs. With ultrasound the pancreas can be directly assessed for evidence of inflammation and the severity of this inflammation can be subjectively assessed (Figure 2). In addition, complications such as pancreatic pseudocysts, peritoneal effusions and gastrointestinal ileus can be identified. Ultrasound also has a role in excluding other intra-abdominal diseases and can be used daily to monitor disease progression.

Figure 2: In this dog with pancreatitis the enlarged and hypoechoic pancreas can be seen with the body of the pancreas identified by the 'x' calipers and the right limb identified by the '+' calipers. Additional changes associated with acute pancreatitis include the irregular pancreatic outline, the hyperechoic peripancreatic mesentery and the free abdominal fluid

Advanced imaging - computed tomography, magnetic resonance imaging and contrast-enhanced ultrasound may aid diagnosis of pancreatitis. They require anaesthesia and/or the administration of contrast agents, are not readily available and are significantly more expensive than other forms of imaging and as such are hard to justify in most cases.


The pathophysiology of pancreatitis involves an initial insult (the type/mechanism of insult is poorly understood) followed by a series of secondary injuries to the pancreas and other organ systems brought about by the release of inflammatory mediators, poor tissue perfusion and loss of gastrointestinal integrity. Therapy targets this secondary injury.  We aim to reduce pancreatic inflammation as well as prevent life-threatening complications such as renal injury, disseminated intravascular coagulation, acute lung injury and other often fatal emergency medicine acronyms (e.g. Systemic inflammatory response syndrome (SIRS), Multiple organ dysfunction syndrome (MODS)).


The severity of pain experienced by dogs with acute pancreatitis is evident to anyone who has encountered these cases.  The extent of pain experienced in cats with acute pancreatitis is less clinically apparent but given the propensity of cats to hide their true feelings, and the pain associated with pancreatitis in humans and other species, we should assume that affected cats also suffer significant pain.

Comprehensive analgesia can be difficult to achieve in severe cases of pancreatitis and in some cases marked pain responses are evident in patients receiving constant rate infusions of fentanyl, ketamine and lignocaine.  For doses and combinations of constant rate infusions for analgesia I find the Veterinary Anaesthesia and Analgesia Support Group CRI website an excellent resource.5 Opioid analgesia is likely to be the first choice in most clinics. Transdermal opioid patches can be a great option, particularly following discharge when other forms of opioid medication are hard to administer.  Typically I would use buprenorphine patches (Norspanâ)in most dogs and in almost all cats (approximately 1mcg/kg/hr for both species) and fentanyl patches in dogs with more severe pain (2-4mcg/kg/hr). There are concerns about the reliability of bioavailability with these patches, particularly in critically ill patients, however, use following discharge is likely to provide some analgesia in a context where there are few other clinical options. It should be noted that NSAIDS are contraindicated in most patients due to pre-existing insults to both the gastrointestinal and renal system.


The role of nausea in canine acute pancreatitis is hard to overlook but even in cats, where vomiting is an uncommon clinical sign, nausea is likely to be a significant contributing factor to anorexia. Maropitant is, for most clinicians, the first choice antiemetic given its potent and multifocal activity, demonstrated visceral analgesia and ability to reduce inflammatory disease (in one experimental study of rats knockout of the NK-1 receptor reduced pancreatic necrosis and acute lung injury in experimentally induced cases of pancreatitis).6Maropitant is also licensed in Australia including recent expansion of this license to include intravenous administration.  I would recommend the use of maropitant in all cases of pancreatitis with a reduced or absent appetite (1mg/kg IV/SC q24h – dogs and cats).  Where anorexia persists, and costs permit, multimodal antiemesis would most effectively be extended with the addition of ondansetron (0.5-1mg/kg IV q8-12h – dogs and cats).

Intravenous fluid therapy

Hypovolaemia and hypoperfusion are significant factors in acute pancreatitis and our ability to give intravenous fluids is perhaps the most powerful tool at our disposal for treating acute pancreatitis. Combinations of crystalloids (e.g. Hartmann’s) and colloids (e.g. voluven®) should be used as required to achieve haemodynamic stability. Fluid requirements vary greatly between patients, thus goal-orientated fluid therapy is strongly recommended with frequent reassessment of parameters such as moistness of mucous membranes, capillary refill time, arterial blood pressure, heart rate, serum lactate levels and body weight. It should be noted that losses to vomiting, diarrhoea and third-spacing can be high in these patients. In practice I would typically start at least 6ml/kg/hr of crystalloids and will continue at this rate until I was satisfied that the patient’s tissue perfusion was adequate.  I would add colloids when there is:

  • A refractory response
  • Significant third-spacing
  • Hypoalbuminaemia

Colloids should be used with great care in cats due to the risk of occult cardiomyopathy (use half the volume you would use in a dog of the same weight). It is also good practice to monitor respiratory rate and cardiac auscultation closely in this species when using high fluid rates.  When used in combination I typically use both boluses of colloids (e.g. 5-10ml/kg prn - dogs) and infusion rates of 1ml/kg/hr (dogs).  When colloids are used maintenance rates of crystalloids are typically halved.

Supportive/symptomatic treatment

There are a selection of supportive measures that can be very beneficial in some patients and most of these involve the gastrointestinal tract. Due to the proximity of the pancreatitis-associated peritonitis to the stomach gastric ileus is a common complication that can cause vomiting/regurgitation, discomfort and inappetence.  In patients with this complication it may be necessary to use a combination of gastric suction via a nasogastric tube and prokinetic drugs. In terms of prokinetic drugs my personal choice with pancreatitis is cisapride which we have compounded into a liquid (10mg/ml) and administer orally at 0.5mg/kg three times daily, this dose is suitable for dogs and cats although ileus is most commonly encountered in dogs. I find this to be more potent than the more readily available metoclopramide which also has some theoretical concerns over possible worsening of pancreatic perfusion due to its dopamine antagonism. However, in some cases both agents are used to attempt to resolve severe ileus.  In such cases I would typically use a metoclopramide intravenous constant rate infusion (2mg/kg/24h) following an initial bolus (0.2mg/kg IV).

The myth of starving the pancreas to allow it to rest has been debunked and early gastrointestinal nutrition is recommended.7 Enteric nutrition provides metabolic support for the critically ill patient, helps resolve gastrointestinal ileus and provides support to the all-important enterocytes which provide intestinal integrity. Where feeding tubes are placed and vomiting is controlled early administration of low-fat liquid food is highly recommended.

Other treatments

Plasma/fresh frozen plasma - this is often cited as a valuable treatment for pancreatitis but benefits have not been established. While some components of plasma may be beneficial, others are pro-inflammatory and detrimental.  Given the potential for side effects and the relatively high cost of plasma it is hard to justify its routine use in acute pancreatitis at this time.8

Antibiotics - the vast majority of cases of pancreatitis in dogs and cats are sterile and the benefits of antibiotic administration is questionable. Even in cases where pancreatic ‘abscesses’ are identified these are usually sterile. In some cases of severe pancreatitis, where there is an overwhelming demand on the immune system and loss of gastrointestinal integrity, secondary septic insult may add to systemic inflammatory disease. In these cases there may be a role for antibiotics. Antibiotics should be reserved for cases with markers of septic involvement such as persistent hypo- or hyperthermia, and cases with neutropenia or severe neutrophilia in unwell patients. Where antibiotics are used they should be broad-spectrum with a particular need to cover the gram-negative bacteria which are most likely to incite marked inflammatory responses.  A suitable first line choice would be enrofloxacin intravenously at 10mg/kg q24h for dogs and 5mg/kg IV for cats (warn the owners of the possible but very low risk of retinopathy).


The prognosis of acute pancreatitis is variable and difficult to predict.  Attempts to produce scoring criteria in dogs have failed to achieve acceptance.  While we do not have a scoring system in cats, certain criteria, namely fPL and hypocalcaemia, are predictive of a worse outcome. While your clinician’s intuition will give you a fair idea of whether it is a severe or mild case it is worth preparing owners of more severely affected patients for a potential lengthy hospital stay and the possibility that their pet may not survive.


In dogs there appears to be a strong link to dietary indiscretion, particularly the feeding of high-fat foods. Thus it is strongly recommended to feed a low-fat diet, such as Hills i/d®, during recovery from pancreatitis. Patients with recurrent episodes should be fed such a diet lifelong, while all patients with a history of pancreatitis should avoid high-fat foods.

In cats there is no known effective method of prevention and we are limited to serial monitoring of clinical signs and fPL with early intervention when flare-ups occur. There is no evidence that dietary management is of benefit in cats. In some cats, pancreatitis may be linked to chronic enteropathy (e.g. small cell lymphoma or inflammatory bowel disease). Where there is suspicion of enteropathy, such as sonographic evidence of small intestinal thickening or a chronic history of vomiting, further diagnostics and treatment are indicated.

Dr Matthew Best MA VetMB FANZCVS
Registered Specialist in Small Animal Medicine
Brisbane Veterinary Specialist Centre

Matthew graduated from the University of Cambridge in 2008. After one year in mixed general practice in the Cotswolds, he moved to Brisbane where he worked for three years in general small animal practice. Matt then joined Brisbane Veterinary Specialist Centre in 2012. He is a Fellow of the Australian and New Zealand College of Veterinary Science and has extensive experience in all areas of small animal internal medicine.  He has also published in international peer reviewed scientific journals.


  1. Haworth MD, Hosgood G, Swindells KL, Mansfield CS. Diagnostic accuracy of the SNAP and Spec canine pancreatic lipase tests for pancreatitis in dogs presenting with clinical signs of acute abdominal disease. Journal of Veterinary Emergency and Critical Care 2014; 24(2): 135-142.
  2. Oppliger S, Hilbe M, Hartnack S, Zini E, Reusch CE, Kook PH. Comparison of serum spec fPL (™) and 1,2-o-Dilauryl-Rac-Glycero-3-Glutaric Acid-(6’-Methylresorufin) ester assay in 60 cats using standardized assessment of pancreatic histology. Journal of Veterinary Internal Medicine 2016; 30(3): 764-70.
  3. De Cock HE, Forman MA, Farver TB, Marks SL. Prevalence and histopathological characteristics of pancreatitis in cats. Veterinary Pathology 2007; 44(1): 39-49.
  4. Caney SMA. Pancreatitis and diabetes in cats. Veterinary Clinics of North America; Small Animal Practice 2013; 43: 303-317.
  5. Veterinary Anaesthesia and Analgesia Support Group. Drug delivery calculators page  http://www.vasg.org/drug_delivery_calculators.htm  Last accessed 21st June 2016.
  6. Bhatia M, Saluja AK, Hofbauer B et al. Role of substance P and the neurokinin 1 receptor in acute pancreatitis and pancreatitis-associated lung injury. Proceedings of the National Academy of Sciences of the United States of America 1998; 95(8): 4760-4765.
  7. Jensen KB, Chan DL. Nutritional management of acute pancreatitis in dogs and cats. Journal of Veterinary Emergency and Critical Care 2014; 24(3): 240-250.
  8. Weatherton LK, Streeter EM. Evaluation of fresh frozen plasma administration in dogs with pancreatitis: 77 cases (1995-2005). Journal of Veterinary Emergency and Critical Care 2009; 19(6): 617-622.

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