ttp://www.bsava.

com REVIEW

Management of acute pancreatitis

in dogs: a critical appraisal with focus
on feeding and analgesia
C. Mansfield and T. Beths

Faculty of Veterinary and Agricultural Sciences, The University of Melbourne, 250 Princes Highway, Werribee, Victoria 3030, Australia

Knowledge about acute pancreatitis has increased recently in both the medical and veterinary
fields. Despite this expansion of knowledge, there are very few studies on treatment interventions in
naturally occurring disease in dogs. As a result, treatment recommendations are largely extrapolated
from experimental rodent models or general critical care principles. General treatment principles
involve replacing fluid losses, maintaining hydrostatic pressure, controlling nausea and providing pain
relief. Specific interventions recently advocated in human medicine include the use of neurokinin-1
antagonists for analgesia and early interventional feeding. The premise for early feeding is to improve
the health of the intestinal tract, as unhealthy enterocytes are thought to perpetuate systemic
inflammation. The evidence for early interventional feeding is not supported by robust clinical trials
to date, but in humans there is evidence that it reduces hospitalisation time and in dogs it is well
tolerated. This article summarises the major areas of management of acute pancreatitis in dogs and
examines the level of evidence for each recommendation.

Journal of Small Animal Practice (2015) 56, 27–39

DOI: 10.1111/jsap.12296
Accepted: 26 May 2014

INTRODUCTION Acute pancreatitis (AP) is considered to be a reversible condi-

tion unless the initial triggers of disease persist, in which case
chronic or recurrent inflammation develops (Holm et al. 2003,
Pancreatitis develops when there is excessive activation of tryp-
sin and other pancreatic proteases within the pancreas, which Stevens et al. 2004). AP is characterised histologically by neutro-
overwhelms local safeguards within the acinar cell (Lasson & philic inflammation or necrosis of the pancreatic or peri-pancre-
Ohlsson 1984, Mansfield 2012). This initial activation may be atic area with no fibrosis or exocrine atrophy present (Newman
due to oxidative stress or hypotension, and is experimentally et al. 2006, Watson et al. 2007, Kalli et al. 2009). Clinically the
worsened by low acinar pH and high intracytosolic calcium con- differentiation between acute necrotising pancreatitis, AP with-
centration (Rinderknecht 1986, Mithofer et al. 1995, Windsor out necrosis and chronic active AP (inflammation and fibrosis
& Hammodat 2000, Noble et al. 2008, Bhoomagoud et al. from a previous insult) is difficult. Therefore, veterinary clinical
2009). Trypsin and chymotrypsin then directly stimulate the nomenclature usually relates to the severity and longevity of clin-
migration of neutrophils to the pancreas with subsequent pro- ical signs rather than to the histological characteristics. The term
duction of reactive oxygen species, nitric oxide, cytokines and mild AP should be used when there is no multisystem failure,
activation of other pathways (complement, kallin–kallikrein and whilst severe AP should refer to the presence of multisystem fail-
renin-angiotensin system) that further perpetuate inflammation ure or development of complications that require a higher inten-
in the pancreatic and peri-pancreatic area (Frossard 1999, Bhatia sity of treatment. Typically, dogs that have severe AP also have
et al. 2000, Keck et al. 2005). Clinical signs of pancreatitis are pancreatic or peri-pancreatic necrosis (Mansfield et al. 2008).
dependent on the degree of local pancreatic inflammation (pain, The reported mortality rate for AP in dogs ranges from 27 to
vomiting and dehydration) and the degree of systemic compli- 58% (Strombeck 1990, Cook et al. 1993, Charles 2007). This
cations (such as cardiac arrhythmias, disseminated intravascular rate may not reflect the mortality in general veterinary practice,
coagulation and acute lung injury). as these reports originate from referral centres and euthanasia

Journal of Small Animal Practice • Vol 56 • January 2015 • © 2015 British Small Animal Veterinary Association 27
 C. Mansfield & T. Beths

for non-medical reasons (i.e. financial) may exert an influence. are intensive in nature, and as such dogs with severe AP may
Even taking these factors into account, AP in dogs has a mor- be better treated in a referral intensive care unit. It should also
tality rate higher than that reported in human studies of 5 to be kept in mind that these are recommendations only, but it is
15% (Al Mofleh 2008). The treatment for AP in dogs is largely hoped that future prospective studies will enable a stronger LOE
extrapolated, either from first principles, experimental studies in to be applied to this common disease.
species other than dogs, or from medical studies.
In this review, each of the major aspects of management of
AP is addressed and assigned an overall level of evidence (LOE) INTRAVENOUS FLUID THERAPY
for each treatment in both humans and dogs (Table 1). The
LOE was classified as follows: level A is based on consistent ran- Vomiting and inappetence result in dehydration in dogs with
domised control trials and cohort studies in different populations AP, which generally requires intravenous (iv) fluid replacement.
of subjects; level B is based on consistent retrospective cohorts, In addition to the systemic effects of dehydration or hypovolae-
experimental cohorts of the same species, case–control studies or mia, the pancreas is susceptible to altered blood flow (Gardner
extrapolated from level A studies; level C is based on case series, et al. 2008). Disturbed pancreatic microcirculation is usually
or extrapolation from level B studies; level D is expert opinion multifactorial in origin and can occur as a result of increased
without explicit critical appraisal or extrapolated from bench-top vascular permeability resulting from inflammatory cytokines,
research or physiological (first) principles (Elwood et al. 2010). and microthrombi formation resulting from hypercoagulability
Initially search engines such as PubMed and Web of Science (Fig 1) (Gardner et al. 2008). There is a theoretical benefit in
were searched for the terms “canine OR dog” and “acute pan- using alkalinising fluids, such as lactated Ringer’s solution (LRS),
creatitis”. This initially identified 1782 articles. After excluding to increase pH and therefore prevent further trypsin activation
articles that were in duplicate, not available in English, written within the acinar cell (Bhoomagoud et al. 2009). Although a
prior to 1965, discussed other diseases such as chronic pancreati- protective effect was not shown in experimental rodent studies
tis or were related to another species, 158 remained. Of these, a (Kellum 2002), one randomised prospective study in humans
total of 133 experimental studies on dogs (ex vivo or in vivo) of did demonstrate that LRS given iv reduced signs of systemic
treatment modalities, 13 reviews, 2 individual case reports, 8 ret- inflammation more than saline (Wu et al. 2011). Further studies
rospective case series and 2 small prospective studies were found. are required to determine whether there is a tangible advantage in
As there is a dearth of well-structured studies in many areas of using LRS as the first-choice crystalloid in dogs with AP (current
management of AP in dogs, medical and experimental studies in LOE in dogs D).
each area were separately reviewed. There are multiple rodent experimental studies that show a
Many of the recommendations given for treatment of severe beneficial effect of dextrans on crystalloid therapy in AP (Don-
and complicated AP require a high level of nursing support and aldson & Schenck 1979, Knol et al. 1983, Schmidt et al. 1993,

Table 1. Assessment of the overall level of evidence for major treatment strategies of acute pancreatitis (AP) in dogs
Treatment intervention Treatment recommendations Level of evidence
Intravenous fluid therapy Lactated Ringers preferable crystalloid B (humans)
Dextrans beneficial if unable to maintain perfusion with crystalloids D (dogs)
No benefit of fresh frozen plasma C (dogs)
A (humans)
C (dogs)
Anti-emetic therapy Metoclopramide potentially detrimental D (dogs)
Maropitant ideal first line treatment B (dogs)
Antibiotics Not required unless suspect bacterial translocation A (humans)
Amoxicillin-clavulanate or ticarcillin first drug of choice if needed D (dogs)
C (dogs)
Gastric cytoprotection Nasogastric suctioning contraindicated A (humans)
Omeprazole first-line drug of choice at 2 to 2·5 mg/kg orally daily in divided doses D (dogs)
C (dogs)
Corticosteroids Hydrocortisone could be considered in cases non-responsive to iv fluid resuscitation B (humans)
D (dogs)
Surgical intervention No indication for surgical intervention with AP unless infection is documented A (humans)
B (dogs)
Pancreatic fluid collections Fluid collections should be aspirated via ultrasound guidance only if associated with pain A (humans)
C (dogs)
Post-recovery treatment Exocrine pancreatic supplementation and a low-fat diet should be given for 4 weeks D (dogs)
Serum triglyceride and cholesterol concentrations should be measured 2 to 4 weeks postrecovery D (dogs)
from AP. If hyperlipidaemic, a low-fat diet should be continued indefinitely, and if necessary lipid-
lowering medications prescribed. If hyperlipidaemia is not present, then the regular diet can be
cautiously reintroduced
Level A is based on consistent randomised control trials and cohort studies in different populations of subjects; level B is based on consistent retrospective cohorts, experimental cohorts of
the same species, case–control studies or extrapolated from level A studies; level C is based on case series, or extrapolation from level B studies; level D is expert opinion without explicit
critical appraisal, or extrapolated from bench-top research or physiological (first) principles. Adapted from Elwood et al. 2010. Further discrimination is given by indicating the species of study

28 Journal of Small Animal Practice • Vol 56 • January 2015 • © 2015 British Small Animal Veterinary Association
 Treatment of acute pancreatitis

1991) or in dogs (Weatherton & Streeter 2009), and it remains

an expensive treatment for veterinary cases. The study in dogs
(Weatherton & Streeter 2009) was a retrospective one and there-
fore had inherent bias, limiting the strength of recommendations
that can be made for FFP. Despite this limitation, it is observed
that administration of FFP should probably be reserved for those
dogs with documented coagulation abnormalities. This lack of
benefit of FFP has a LOE D in dogs, and A in humans.

ANTI-EMETICS

Vomiting in dogs with pancreatitis is likely to be both centrally

mediated owing to the presence of circulating emetic agents and
peripherally mediated owing to ileus, peritonitis, and pancre-
atic distension (Elwood et al. 2010). Experimental rodent mod-
els have shown that dopamine infusion improves the outcome
in AP and ameliorates the inflammatory severity of the disease
(Karanjia et al. 1990). There is therefore a theoretical disadvan-
tage in giving metoclopramide (a dopaminergic antagonist) to
dogs with AP, although this is clinically unproven (LOE dogs D).
Maropitant (Cerenia, Pfizer) blocks the neurokinin-1 (NK1)
receptor and substance P production; and is an effective anti-
emetic agent that blocks centrally and peripherally mediated
emesis (Benchaoui 2007, De la Puente-Redondo et al. 2007a,b,
Conder 2008, Sedlacek et al. 2008, Rau et al. 2010). Maropitant
is also the only anti-emetic discussed in this review specifically
labelled for that use in dogs in the UK. Substance P contributes
to the development of visceral pain and increased capillary per-
meability (Frossard & Pastor 2002). When the NK1 receptor is
blocked experimentally, there is no difference in the amount of
pancreatic inflammation produced, but distantly mediated lung
injury is reduced in rodents (Pastor & Frossard 2001). Although
there is a danger of direct extrapolation, the NK1 receptor func-
tion is considered the same in dogs as in humans (Leffler 2009).
FIG 1. Diagrammatic representation of circulatory changes in pancreatic
Therefore, there may be additional benefits such as reduction of
circulation with disease. ICAM Intracellular adhesion molecule, PMN visceral pain and lung injury with the use of maropitant. Although
Neutrophils. Reproduced with permission from Mansfield 2012 there is no evidence of these adjunctive benefits of maropitant in
dogs with AP to date, the authors consider that this should be the
preferred first-line anti-emetic (LOE B in dogs). Additional anti-
1996). Administration of dextrans has been associated with alter- emetic agents such as the serotonergic antagonists (e.g. ondan-
ation in haemostasis (Mehler et al. 2004). That being said, addi- setron) can be added as necessary to improve nausea or emesis
tional therapy with dextrans, hetastarch or hypertonic saline (at a control, although they remain expensive.
low bolus dose), may be beneficial in those dogs that have severe Even dogs with AP that are not showing overt signs of nausea
disease (current LOE in dogs: C). or vomiting should be treated with an anti-emetic, especially in
the early stages to encourage voluntary eating. Clinical signs of
Plasma nausea include repeated licking of lips and swallowing attempts
Purported benefits of plasma transfusion in treatment of AP or obvious aversion to food.
include replacement of circulating α-macroglobulins, coagu-
lation factors and anti-inflammatory factors (Weatherton &
Streeter 2009). It is unlikely that any benefit of plasma is because ANTIBIOTICS
of its colloid-like properties, as fresh frozen plasma (FFP) has
only approximately 20 to 30% of the oncotic properties of syn- Potential reasons for administration of antibiotics to dogs with
thetic colloids (Weatherton & Streeter 2009). Despite an experi- AP include treatment of infected pancreatic necrosis or treatment
mental benefit of FFP in rats (Leese et al. 1988), there has been of bacterial translocation (Wu & Conwell 2010b). Bacterial
no proven benefit in humans (Leese et al. 1987, Leese et al. translocation has been documented in dogs with experimentally

Journal of Small Animal Practice • Vol 56 • January 2015 • © 2015 British Small Animal Veterinary Association 29
 C. Mansfield & T. Beths

induced pancreatitis (Kazantsev et al. 1994, Qin et al. 2002a), none of which showed any benefit and many showed prolonga-
but has not been definitively documented in naturally occurring tion of pain and nausea (Levant et al. 1974, Naeije et al. 1978,
disease. If bacterial translocation were to occur, experiments sug- Field et al. 1979, Fuller et al. 1981, Loiudice et al. 1984, Navarro
gest that the bacteria would originate from the small intestine et al. 1984, Sarr et al. 1986). The physical presence of a nasogas-
(Fritz et al. 2010). Clinically, it is difficult to have definitive cri- tric tube across the gastro-oesophageal sphincter may also predis-
teria for suspecting bacterial translocation as the severe (sterile) pose to the development of severe oesophagitis. As such, the use
inflammation that accompanies AP often results in pyrexia and of indwelling nasogastric tubes or repeated nasogastric suctioning
white cell changes that are indistinguishable from infection (Hess is not recommended in dogs with AP (LOE humans A; LOE
et al. 1998, Mansfield et al. 2008). In general, signs of poor gut dogs D).
mucosal health (melaena and haematochezia) combined with
prolonged fasting and/or hypotension could increase suspicion of
bacterial translocation, and then drugs such as amoxicillin–clavu- CORTICOSTEROIDS
lanate that are broadly effective against gut pathogens should be
given parenterally (LOE dogs C), unless a documented infection Corticosteroids may exert multiple positive benefits in AP by
with a different antimicrobial susceptibility has been confirmed. inhibiting the release of pro-inflammatory mediators, decreas-
The routine use of prophylactic antibiotics in dogs without signs ing sequestration of neutrophils in the pulmonary vasculature, as
of concern may lead to increased community resistance to antibi- well as reducing adhesion of primed neutrophils to the endothe-
otics, and should be avoided if possible (LOE dogs D). lial surface of pulmonary vasculature, pulmonary vascular per-
meability, and release of elastase and free radicals from adherent
neutrophils (Sun et al. 2007). Experimental in vitro and in vivo
GASTRIC ACID SUPPRESSION AND NASOGAS- models demonstrate that dexamethasone increases the expres-
TRIC SUCTIONING sion of pancreatitis-associated protein (PAP) (Kandil et al. 2006).
PAP is upregulated in pancreatic inflammation and is thought to
Reduction of gastric acidity medically or via physical suctioning have multiple protective effects (Iovanna et al. 1991, Zenilman
of gastric contents is recommended by many in the treatment of 1996, Ortiz et al. 1998, Heller 1999). Corticosteroids have been
canine AP (Stewart 1994, Williams 1994, Watson 2004, Kalli removed from the list of drugs that are considered to cause pan-
et al. 2009). It is proposed that reduction of gastric acid pro- creatitis in humans, and similarly, they are not believed to cause
duction could lead to decreased pancreatic exocrine stimulation pancreatitis in dogs (Parent 1982, Fittschon & Bellamy 1984,
and that AP predisposes to the development of gastric mucosal Bang et al. 2008). Currently, a number of prospective trials are
ulceration as a result of hypovolaemia and localised peritonitis being carried out to evaluate the potential benefit of glucocor-
(Williams 1994). One experimental study in rats showed that ticoids in humans with severe AP, but their routine use is not
pantoprazole reduced inflammatory changes and leakage within recommended yet.
acinar cells (Hackert et al. 2010), but there was no direct effect of During acute illness, the hypothalamic–pituitary axis is stimu-
proton pump inhibitors on pancreatic exocrine secretion in vitro lated, but in approximately 10 to 20% of critically ill and 60%
(Cai et al. 2007). This would suggest that this group of drugs of humans with septic shock, this pathway becomes impaired
may directly reduce pancreatic inflammation in a way that is not (Marik 2008). This altered adrenal function has been termed
associated with reduced pancreatic enzyme secretion. critical illness-related corticosteroid insufficiency (CIRCI), but
Currently, there is no evidence that reducing gastric acidity it remains a subject of some debate. Mechanisms that lead to
improves outcome in dogs with AP. However, if there is clini- CIRCI are complex and poorly understood, but CIRCI occurs
cal evidence of gastric ulceration (substantial haematemesis, effectively when there is adrenal insufficiency along with tissue
melaena) or oesophagitis (repeated eructations, regurgitation), resistance to the effects of corticosteroid, owing to a prolonged
then gastric acid suppression is indicated. Oral doses of omepra- and severe pro-inflammatory state (Marik 2008). CIRCI appears
zole, a proton pump inhibitor, have been shown to be the most to occur most frequently in diseases that alter lecithin-cholesterol
effective at increasing gastric pH for the longest period of time acyltransferase (LCAT). LCAT converts free cholesterol into cho-
in dogs compared with famotidine, pantoprazole, and ranitidine lesteryl ester and produces high-density lipoproteins. The role of
when given every 12 hours (Bersenas et al. 2005, Tolbert et al. LCAT in canine AP is unknown, but could theoretically contrib-
2011). Recent work would suggest that doses of oral omeprazole ute to the lipid perturbations commonly seen in severe AP.
should be increased up to 2·5 mg/kg day, in divided doses (Tol- CIRCI causes hypotension and a poor response to fluid or
bert et al. 2011; LOE B). The potential direct effect of proton vasopressor therapy; it is in the subgroup of humans with poor
pump inhibitors on pancreatic inflammation, combined with response to resuscitative measures (fluid and vasopressor therapy)
their greater efficacy, would suggest that they are first-line gastric and those with acute lung injury, where cortisone replacement
cytoprotective choices in dogs with AP despite not being licensed therapy appears to be the most effective (Marik 2008). Low-dose
specifically for use in dogs in the UK and being more expensive hydrocortisone tapering over 2 weeks is the currently recom-
than H2 antagonists (LOE C). mended treatment for humans with septic shock and CIRCI,
Multiple randomised clinical trials are available for assessing whilst methylprednisolone is recommended for those with acute
nasogastric suctioning in humans with mild to moderate AP; lung injury.

30 Journal of Small Animal Practice • Vol 56 • January 2015 • © 2015 British Small Animal Veterinary Association
 Treatment of acute pancreatitis

These treatment recommendations have not been extended to essential to optimise its management. Behavioural and physi-
humans with AP to date (Muller et al. 2006, Peng et al. 2009), ological characteristics associated with pain in dogs and cats have
and there is no published evidence that CIRCI occurs in dogs been described (Mathews 2000, Price & Nolan 2007) and differ-
with AP. There may be a potential reason for using low-dose ent pain scoring systems have been developed to help the veteri-
hydrocortisone in dogs with severe AP that have poor systolic narian with pain assessment. A guide to identify pain has been
pressures and minimal response to fluid resuscitation (LOE B developed by the WSAVA Global Pain Council (http://www.
humans, D dogs); however, it is believed that optimisation of wsava.org/sites/default/files/Guidelines%20for%20the%20
other aspects of AP management should be completed before Recognition%2C%20Assessment%20and%20Treatment%20
prospective analysis of corticosteroid therapy is carried out. of%20Pain.pdf ). The most commonly used pain scoring systems
are descriptive and rely on a highly subjective interpretation of
behavioural signs (Dobromylskyj et al. 2000). To improve the
ANALGESIA quality of the pain assessment, composite scoring systems such
as the dynamic and interactive visual analogue scale (DIVAS)
Pain is a common clinical sign of AP and is manifested in dogs have been developed (Lascelles et al. 1997). The DIVAS scoring
typically with a crouched appearance and guarding of the abdo- system consists of three scaled components: observation of the
men on palpation (Hess et al. 1998). Pain is likely to be medi- animal from a distance; measurement of the animal’s response
ated as a result of local effects whereby the inflamed and enlarged to interaction; and response to wound (or in the case of AP,
pancreas itself causes pain, or by subsequent amplification of abdominal) palpation. The addition of these three components
visceral pain. From a simplistic point of view, the pain pathway gives a number that defines the level of (dis)comfort in the ani-
is divided into a nociceptive ascending and an anti-nociceptive mal. Unfortunately, even this pain-scoring scale looks at only one
descending pathway. The former starts at the periphery, in this aspect of the pain experience: the intensity.
case the inflamed and enlarged pancreas, and sends informa- Multidimensional scales published for use in dogs that con-
tion in the dorsal horn through a first set of nerve fibres with sider aspects other than pain intensity include the Melbourne
co-release of amino acids (glutamate and aspartate) and neuro- Pain Scale (Firth & Haldane 1999) and the Glasgow Composite
peptides (substance P, neurokinin A and calcitonin gene-related Pain Scale (GCPS) (Holton et al. 2001). Amongst these, only the
peptide) (Lemke & Creighton 2010). At this level, intense and/ GCPS has been designed using psychometric principles (estab-
or prolonged afferent input may result in the activation of the lished process of item selection, questionnaire construction and
N-methyl-D-aspartate (NMDA) receptor involved in central testing for validity, reliability and sensitivity). However, the origi-
sensitisation. From the dorsal horn, a second set of neurons carry nal GCPS was too long to be of use in a busy clinical practice, and
the nociceptive (painful) information to the thalamus where a so a shorter form has since been assessed and validated (Morton
third group of neurons send the information to the cortex (Price et al. 2005, Murrell et al. 2008). The short form of the GCPS is
& Nolan 2007). The descending anti-nociceptive pathway starts accessible to practitioners online (http://www.gla.ac.uk/schools/
at the supraspinal level and projects to neurons in the dorsal horn vet/research/painandwelfare/downloadacutepainquestionnaire/);
of the spinal cord. This pathway modulates the nociceptive input it provides veterinarians with a practical tool that might be of
through different neurotransmitters such as opioids, norepineph- clinical relevance to manage AP.
rine, α2-agonists and serotonin (Lemke & Creighton 2010). Even using this abridged GCPS, it is possible for factors to
Even if animals do not display typical signs of pain, it is sen- influence the correct assessment of pain recognition. It is recom-
sible to assume that there exists a degree of pain in all dogs with mended that these factors be taken into account when assessing
AP. Accurate identification and characterisation of this pain is pain in dogs with AP (Table 2), and a few key points to facilitate

Table 2. Confounding factors that may interfere with pain assessment of animals, and key points which may facilitate
with accurate assessment
Factors that may affect pain assessment Key points to facilitate pain assessment
Altered environment Good knowledge of species-specific behaviour
(e.g. in hospital, the presence or not of the owner, the presence of other Knowledge and comparison of the behaviour before with after the trauma
animal of the same species or not) or illness
Species differences Response to analgesic treatment is the best marker for accurate diagnosis
(e.g. “Normal” comportment for given species, varied reaction to pain of pain
between species) Behaviour is easily altered by age, illness or drugs
Within-species variation Assess interaction with owner or handler
[e.g. Individual dogs react differently (Labrador versus Greyhound)] Assess response to abdominal palpation or manipulation
Drugs might alter behaviour The assessor must be experienced in pain assessment
(e.g. sedative agents do not always provide analgesia although case
If possible, the same person should assess the animal at least on a daily
appears comfortable; analgesic drugs might provide sedation)
basis during hospitalisation
Animal should reassess frequently and a good knowledge of the length of
action of particular analgesic agent or procedure must be well known

Journal of Small Animal Practice • Vol 56 • January 2015 • © 2015 British Small Animal Veterinary Association 31
 C. Mansfield & T. Beths

pain recognition are provided. By determining a level of pain, an tory depression described with these drugs is rarely clinically
appropriate level of analgesia can be initiated (Table 3). However, significant (Kerr 2007). Decreased gastric emptying time and
none of the analgesic agents recommended have been evaluated intestinal propulsive activity have been demonstrated in dogs as
in dogs with spontaneous AP or in experimental canine models. well as increased sphincter tone (pylorus or biliary sphincter),
Hence, the LOE for these recommendations is poor (level D), predominantly with the full µ-agonists, and is the biggest com-
and the recommendations are based on the authors’ professional plication associated with this group of analgesic agents in dogs
opinion. Owing to the potential severity of the pain associated with AP. Morphine should be avoided with conditions of the gall
with AP, a multimodal approach to pain treatment is advised. bladder and biliary tract. Pethidine, fentanyl or butorphanol do
This methodology involves the use of analgesic agents influenc- not increase the pressure in the bile duct to the same extent as
ing the pain process through different mechanisms, allowing for seen with morphine and can therefore be used (Kerr 2007). Fen-
better pain control, lower drug dosages and less potential side tanyl, a synthetic opioid 100 times as potent as morphine, can be
effects (Dobromylskyj et al. 2000). administered iv and transdermally (fentanyl patches). Unfortu-
Analgesic agents can be classified as opioids (full and partial nately, fentanyl’s systemic absorption from transdermal patches
µ-agonist); non-steroidal anti-inflammatory drugs (NSAIDs), is erratic and will vary with body temperature, peripheral circula-
NMDA antagonists (e.g. ketamine), local anaesthetic agents, tion and hydration (Lemke & Creighton 2010). Even with good
α2-adrenoceptor agonists and adjuvant drugs (e.g. tramadol and hydration and normothermia, the onset time is slow with a 12-
gabapentin). Recommended routes of administration and dos- to 24-hour lag time before effective plasma concentrations are
ages are detailed in Table 4. Because of the presence of hypovo- reached which can last for 3 to 5 days. Fentanyl has a profound
laemia and dehydration in the majority of dogs with AP, NSAIDs negative effect on gastrointestinal motility, and so is seldom used
and α2-adrenoceptor agonists are not recommended and will not in the management of AP.
be discussed further. In a rat model of AP, it was suggested that NMDA receptors
The analgesic effect of opioids is provided mostly through were involved not only in initiation but also in the maintenance
their action in the central nervous system on the µ and δ recep- of central sensitisation during visceral inflammation (Zhang
tors (spinal and supra spinal) and the κ receptor (spinal) (Lemke et al. 2004). Ketamine is the most potent and specific NMDA
& Creighton 2010). The full µ-agonist opioid agents (e.g. mor- antagonist in clinical use today (Berti et al. 2009) and plays a
phine, methadone, hydromorphone, meperidine and fentanyl) role in the reduction of central sensitisation (Gaynor 2008), and
are considered the most effective analgesics of the group and are may help reduce nociception from intra-abdominal organs and
usually used to treat moderate to severe pain, while the partial visceral peritoneum (Berti et al. 2009). Ketamine has an opioid-
µ-agonist (e.g. buprenorphine) and the µ-antagonist κ-agonist sparing effect allowing a decrease in morphine consumption
(e.g. butorphanol) are less effective and are used for milder (Gaynor 2008). Ketamine can be administered as a continuous
pain level (Lemke & Creighton 2010). Respiratory depression rate infusion (CRI), with or without a loading dose, adjunctively
has been reported with the use of all these agents, particularly to traditional analgesia. The dose for ketamine infusion being so
the µ-agonists. However, at recommended analgesic doses and low, it is very uncommon for animals to develop behavioural or
unless used concomitantly with other central nervous system cardiovascular effects (Gaynor 2008). Although there is no study
depressants or in animals with respiratory disease, the respira- looking at the effect of long-term ketamine infusion on dogs, a

Table 3. An outline of the levels of pain that are potentially manifested in dogs with acute pancreatitis, as adapted from
the Glasgow Composite Pain Scale and recommended analgesia
Anticipated levels of pain associated with acute pancreatitis Potential analgesic combination Level of evidence
Mild Quiet but responsive to surroundings; Buprenorphine or methadone (or other full µ-agonist) at high-end of D (dogs)
unsettled; looks around when abdomen dosage and frequency, reducing down once pain well controlled
is palpated
Moderate Decreased response to surroundings Buprenorphine or methadone (or other full µ-agonist) at high-end of D (dogs)
or stimuli; slow or reluctant to move; dosage and frequency, PLUS Lidocaine and Ketamine infusion.
restless; stretching of abdomen, look- Once pain well controlled, reduce ketamine infusion first until 5
ing around at abdomen; flinches on µg/kg/minute then stop, then reduce lidocaine until 25 µg/kg/
abdominal palpation minute then stop, then reduce dosage and frequency of opioid.
Severe to Non-responsive to stimuli; refuses to Epidural morphine or fentanyl infusion PLUS lidocaine/ketamine D (dogs)
excruciating move or get up; screams, cries or infusion. Once pain well controlled, change epidural to opioid as
snaps when tries to get up or abdomen above, then reduce ketamine infusion first until 5 µg/kg/minute,
palpated stop and then reduce lidocaine until 25 µg/kg/minute, then stop,
and then reduce dosage and frequency of opioid.
Unexpected exac- Assess for pancreatic fluid collection and aspirate via ultrasound C (dogs)
erbation of pain guidance
Adjunctive Added with any level of pain Gabapentin D (dogs)
management Added if opioids associated with Methylnaltrexone D (dogs)
decreased gastrointestinal motility C (humans)
LOE Level of evidence
The LOE is determined as described in Table 1

32 Journal of Small Animal Practice • Vol 56 • January 2015 • © 2015 British Small Animal Veterinary Association
 Treatment of acute pancreatitis

Table 4. Suggested doses for analgesic agents for dogs with acute pancreatitis
Drug Dose Duration of action Comment
Full µ-agonist
Morphine 0·1 to 0·5 mg/kg, im, sc 4 to 6 hours Caution: histamine with iv injection
0·1 mg/kg/hour CRI
0·1 mg/kg epidural 12 to 24 hours
Hydromorphone 0·05 to 0·15 mg/kg iv, im, sc 2 to 6 hours
Methadone Dog: 0·1 to 1 mg/kg iv, im, sc 2 to 4 hours
Fentanyl 2 µg/kg iv bolus 0·3 hours
0·2 to 0·8 µg/kg/minute CRI
0·003 to 0·005 mg/kg/hour Patches Inconsistent efficacy
Remifentanil 0·2 to 0·8 µg/kg/minute CRI
Ketamine
Ketamine 5 to 20 µg/kg/minute CRI In addition to other analgesic agents
Local Anaesthetic
Lidocaine 25 to 50 µg/kg/minute CRI
1 to 2 mg/kg epidural 2 to 4 hours Caution muscle paralysis
Bupivacaine 1 to 2 mg/kg epidural 4 to 6 hours Caution muscle paralysis
Partial µ-agonist
Buprenorphine 10 to 40 µg/kg, iv, im 6 to 8 hours Generally start at a higher dose and frequency, then taper down if
possible
iv Intravenous, CRI Continuous rate infusion, im Intramuscular, sc Subcutaneous

study of dogs undergoing forelimb amputation showed no side In human medicine, gabapentin is an anticonvulsant that has
effects when ketamine was used intra-operatively at 10 µg/kg/ been shown to provide effective analgesia for neuropathic pain
minute followed with ketamine postoperatively at a 2 µg/kg/ and postoperative abdominal surgeries. The anti-nociception
minute rate for up to 20 hours, apart from dysphoria in two dogs obtained with gabapentin and its successor, pregabalin, results
(Wagner et al. 2002). from inhibiting the release of excitatory neurotransmitters (sub-
Lidocaine is a local anaesthetic that reversibly blocks volt- stance P and calcitonin gene-related peptide) at the level of the
age-gated sodium channels, and thereby prevents membrane dorsal horn by binding on the α2-δ1 subunit of presynaptic volt-
depolarisation; it is usually administered locally to block nerve age-gated calcium channels. In veterinary medicine, the use of
conduction. When administered as an infusion, lidocaine exerts gabapentin has expanded to treat chronic cancer pain, chronic
analgesic effects that appear to be peripheral and central in origin neuropathic pain and perioperative pain in dogs (Lamont 2008).
(Devor et al. 1992, Jaffe & Rowe 1995). In humans, lidocaine has Because of the potential for substance P to contribute to pain
been shown to improve bowel function, decrease postoperative development in AP (Frossard & Pastor 2002), the use of this
pain and reduce opioid consumption following major abdomi- drug in dogs with severe pain is theoretically sound. The use of
nal surgery (Lamont 2008, Vigneault et al. 2011). In addition, gabapentin is preferred to tramadol when managing pain once
lidocaine also has anti-inflammatory properties by reducing the the animal is discharged (LOE D).
liberation of superoxide anions, a common pathway of inflam-
mation (Hollmann et al. 2001, Cassuto et al. 2006). These ben-
efits make it an attractive analgesic option in dogs with severe NUTRITION
pain resulting from AP.
Tramadol is a synthetic codeine analogue that is a weak Traditional management
µ-agonist and a serotonin and noradrenaline reuptake inhibitor, The role of nutrition in the treatment of AP has gained a lot
by which it contributes to the reduction in nociceptive trans- of attention recently in both human and veterinary medicine,
mission within the spinal cord. Tramadol is available in oral and and heralded a change of direction in management (Table 5).
parenteral form, and has been shown to have an analgesic efficacy The nutritional challenges of AP include that it is a catabolic
comparable with that of morphine when administered prior to disease with significant nitrogen losses; ileus often complicates
ovariohysterectomy (Mastrocinque & Fantoni 2003). Common feeding; and pancreatic necrosis can increase nutritional require-
side effects associated with the agent are sedation, inappetence ments (Thomson 2006). Initially in human (and veterinary)
and dysphoria, and titration of the dose to minimise those effects gastroenterology, the consensus was to “rest” the pancreas based
is advised. Dosing guidelines are based on human extrapolation, on the assumption that ongoing pancreatic secretion would
and the recommended dose in dogs is 3 to 5 mg/kg twice or thrice perpetuate pancreatic inflammation (Stewart 1994, Williams
a day, while one study (KuKanich & Papich 2004) reported in 1994). It was subsequently demonstrated experimentally in
the dog that a dose of 5 mg/kg four to five times a day was neces- four different rodent models that exocrine pancreatic secretion
sary to reach analgesic plasma concentrations. At this time, there actually decreased during pancreatitis (Niederau et al. 1990).
are no published pharmacokinetic data in dogs for dosage guide- Additionally, the gastrointestinal tract itself is now thought to
lines for the slow release formulation. be a major contributor to the systemic inflammatory state dur-

Journal of Small Animal Practice • Vol 56 • January 2015 • © 2015 British Small Animal Veterinary Association 33
 C. Mansfield & T. Beths

Table 5. Assessment of the level of evidence for factor for death was a prolonged period of anorexia prior to the
nutritional management of acute pancreatitis, as initiation of TPN.
described in Table 1
Nutritional assumptions Level of evidence Current management principles in humans
Total parenteral nutrition confers a poor prognosis B (humans) Despite most consensus statements in human gastroenterology
in AP C (dogs) supporting the notion of early enteral feeding in severe AP, few
Total parenteral nutrition increases rate of complica- B (humans) clinical studies effectively compare enteral nutrition with full
tions in AP B (dogs)
Early enteral nutrition improves survival in AP com- B (humans) pancreatic rest (Table 5) (Mirtallo et al. 2012). One small study
pared with intestinal rest D (dogs) suggested that enteral feeding decreased mortality and the rate
Early enteral nutrition improves survival in AP com- A (humans) of septic complications compared with iv fluid therapy alone,
pared with total parenteral nutrition D (dogs)
Early enteral nutrition decreases hospitalisation time A (humans)
albeit with no difference in hospitalisation duration or the rate
in AP D (dogs) of non-septic complications (Pupelis et al. 2001). Another study
Early enteral nutrition decreases complication rates A (humans) comparing intestinal rest with enteral feeding showed an increase
in AP B (dogs) in gut permeability in humans fed via a nasojejunal tube, but
Gastric (or oesophageal) feeding is as well tolerated A (humans)
as jejunal feeding in AP C (dogs) no difference in inflammatory markers (Powell et al. 2000). This
Enteral nutrition may be used in the presence of A (humans) was postulated to be because of increased mucosal blood supply.
pancreatic complications such as fistulas, ascites D (dogs) However, mortality, complication rate and hospitalisation dura-
and pseudocysts.
A small peptide-based medium-chain triglyceride A (humans)
tion were not assessed.
(MCT) oil formula may improve tolerance of enteral C (dogs) Most of the experimental and clinical nutritional studies in
nutrition humans initially assessed nutrition delivered into the jejunum.
Attainment of full resting energy requirements is not A (humans)
essential to improve outcome C (dogs)
This was based on the demonstration that jejunal administration
If enteral nutrition is not tolerated, then some form A (humans) of nutrients did not stimulate exocrine pancreatic production of
of parenteral nutrition should be instituted after 5 D (dogs) digestive enzymes, and also stimulated production of polypep-
to 7 days of anorexia tide YY, somatostatin and other substances that inhibit pancre-
AP Acute pancreatitis, MCT Medium-chain triglyceride
atic secretion (Ioannidis et al. 2008). However, multiple studies
in humans have shown that nasogastric feeding is safe and well
tolerated, and a cheaper and easier alternative to insertion of a
ing AP, particularly if it is not supplied with luminal nutrients, nasojejunal feeding tube (Eatock et al. 2005, Kumar et al. 2006,
with amino acids the major respiratory fuel that is required by Petrov et al. 2008).
the enterocytes (Flint & Windsor 2003). In humans and ani- One of the major perceived drawbacks of enteral feeding in
mal experimental models, it has been shown that fasting leads humans with AP is the possibility of pain associated with feeding.
to intestinal mucosal atrophy (King & Kudsk 1997, Hernandez One study assessed pain associated with feeding in humans with
et al. 1999), an increased rate of enterocyte apoptosis in the intes- mild AP (Chebli et al. 2005). They found that 25% of patients
tine (Fukuyama et al. 2001), changes in mucin composition, and had some pain in the 1st or 2nd day of oral feeding, but this was
decreased glutamine and arginine transport (Sarac et al. 1994). associated with the presence of pancreatic fluid collection. One
Conversely, nutrition delivered directly to the intestine decreased study assessed pain in humans with AP when fed orally com-
villus atrophy (Kotani et al. 1999), reduced bacterial transloca- pared with that via a nasojejunal tube, and found no differences
tion and decreased pancreatic inflammation in canine models of (Pandey et al. 2004). A very recent (but small) study showed
AP (Kotani et al. 1999, Qin et al. 2002a,b, 2003, 2007). Survival decreased pain levels and decreased requirements for opiates in
was not assessed in these studies. humans with AP fed early compared with those given intestinal
To counteract the negative nitrogen balance in AP, total par- rest (Petrov et al. 2012).
enteral nutrition (TPN) was historically recommended in severe According to a consensus review, immunonutrition cannot
cases in both the human and veterinary fields. TPN has been currently be recommended in humans with AP (Nathens 2004),
shown to impair humoral and cell-mediated immunity, magnify as no benefit with supplemented glutamine, arginine, tributyrin
the pro-inflammatory response, and increase bacterial transloca- or omega-3 fatty acids was observed (Pearce et al. 2006). This is
tion and infection rate in critically ill humans (Marik & Pinsky despite a large body of theoretical data supporting the benefit
2003). Meta-analysis also shows that TPN worsens the prognosis of glutamine supplementation for enteral health (Souba et al.
in humans with AP (Petrov & Zagainov 2007). There have been 1990). Additionally, a recent randomised, double-blind, placebo-
few reviews on the clinical efficacy of TPN in any specific con- controlled study conducted in Holland in humans with severe
dition in dogs. One study identified a mortality rate of nearly AP assessed probiotic usage (Besselink et al. 2008). The mortality
50% in over 200 dogs that received TPN, along with a high rate rate was significantly greater in the probiotic group, with a rela-
of metabolic (70%), mechanical (25%) and septic (5%) compli- tive risk of 2·53. The biggest cause of death was multiple organ
cations (Reuter et al. 1998). A more recent study showed that dysfunction, although three patients died of bowel ischaemia.
complications of peripheral and centrally administered paren- Death was not related to aetiological classification or the presence
teral nutrition bore no relationship with the outcome (Queau of necrosis. However, the addition of medium-chain triglycerides
et al. 2011) However, this same study also determined that a risk is recommended in humans (Mirtallo et al. 2012).

34 Journal of Small Animal Practice • Vol 56 • January 2015 • © 2015 British Small Animal Veterinary Association
 Treatment of acute pancreatitis

Veterinary nutritional management 2008), which has also been extrapolated to dogs (LOE D). RER
In one randomised, prospective study of enteral nutrition inter- is calculated on the lean bodyweight (BW) of the animal using
vention in dogs with parvoviral enteritis, administration of nutri- the following formula: BW greater than 2 kg and less than 25 kg:
tion via a naso-oesophageal tube resulted in an earlier clinical 30 × BW (kg) + 70 kcal/day; and if less than 2 kg or greater
improvement in dogs but no difference in survival (Mohr et al. than 25 kg then 70 × BW0.75. When starting feeding, on the first
2003). In a prospective pilot study in dogs with severe AP, day a maximum of 25% of the calculated RER should be given,
oesophageal feeding was well tolerated and safe, albeit with a very each feed should not be more than 5 to 10 mL/kg BW, and food
small sample size (Mansfield et al. 2011). Compared with TPN should be given at approximately 1 minute per 5 mL of food
in that study, there was a more rapid reduction in clinical sever- (Saker & Remillard 2010). If this is well tolerated, then the per-
ity and inflammatory markers; however, no difference in survival centage of RER can be increased by up to 25% per day, and the
was identified. Large scale multicentre randomised prospective volume of each feed also increased.
studies are required to fully evaluate the benefits of enteral nutri- In critically ill humans requiring mechanical ventilation, early
tion in dogs. enteral nutrition lowered mortality rates but increased the risk of
Based on the medical consensus, it is recommended that dogs pneumonia (Artinian et al. 2006). The development of aspira-
with mild AP (no systemic complications) be fasted until they are tion pneumonia appears to be one of the largest complications
able to eat voluntarily, unless they have reached 5 days of anorexia of enteral feeding in dogs with AP. Steps to minimise this risk
(including the pre-hospital period), in which case enteral feeding include feeding only when the animal is in sternal position or
should be initiated. In dogs with severe AP, interventional feed- sitting upright, encouraging the animal to move around (walk)
ing (through a naso-oesophageal or oesophageal feeding tube) after the feeding (or have the dog held upright for 10 to 15 min-
should be instituted as soon as possible. utes after feeding) and intermittent bolus feeding rather than
There is no current recommendation for the type of food to be continuous infusion. In addition, avoidance of full mu opioids
administered in this acute setting. Although studies have shown that decrease mentation and gastrointestinal motility aids in the
no difference in dietary fat content on pancreatic secretion in successful introduction of feeding.
healthy dogs (Manas et al. 1996, James et al. 2009), avoidance of
high-fat diets in dogs with AP is logical as many of the animals
are hyperlipidaemic. Given this, veterinary convalescent diets TREATMENT OF LOCAL COMPLICATIONS
may be too high in fat for dogs with AP and concurrent hyper-
lipidaemia (Table 6). Alternative products such as human liquid Acute fluid collections are defined in the human medical litera-
convalescent diets supplemented with protein could be given if ture as fluid accumulations within the pancreatic parenchyma that
naso-oesophageal tubes are being used, which generally have a develop within 6 weeks following AP (Wu & Conwell 2010a). A
small lumen and require a very liquid consistency. If an oesopha- pseudocyst, on the other hand, develops at least 6 weeks after AP,
geal tube is inserted, then a low-fat, high-fibre diet that meets does not contain an epithelial lining and its contents are com-
the requirements set out in Table 6 could be blended and given posed of amylase-rich pancreatic secretion, generally occurring
through the tube easily. To date, there is no evidence that sup- in milder cases (Wu & Conwell 2010a). The term acute fluid
plementation of balanced veterinary diets with medium-chain collection is, therefore, the most suitable term for the local pan-
triglycerides or glutamine, or provision of glutamine alone enter- creatic complications that occur in dogs, although inspissated
ally, will result in clinical improvement in dogs with AP. pancreatic tissue that develops 2 to 3 weeks following AP may be
There is also no evidence that achieving full resting energy termed a phlegmon (Charles 2007).
requirements (RER) is necessary to confer any positive effect Current medical recommendations are to not surgically
on outcome in humans with AP (Nathens 2004, Petrov et al. debride sterile fluid collections, and if infection is documented,

Table 6. Recommendations for assisted (enteral tube) feeding in dogs and common convalescence foods available for use
in dogs
Component Dog requirements (as reported Human liquid Hills AD convalescent Royal Canin recovery
in Saker & Remillard 2010) convalescent diets* tins diet
Caloric density 1 kcal/mL 1 kcal/mL 1·15 kcal/g undiluted† 1·18 kcal/g undiluted†
Digestible carbohydrate days 0 to 2 2 to 4 g/100 kcal 13·4 g/100 kcal 3·2 g/100 kcal 1·3 g/100 kcal
Digestible carbohydrate days 3+ 6 to 10 g/100 kcal
Protein 5 to 12 g/100 kcal 3·27 g/100 kcal 9·2 g/100 kcal 10·5 g/100 kcal
Arginine ≥146 mg/ 100 kcal Unable to determine 495 mg/ 100 kcal 590 mg/100 kcal
Glutamine ≥500 mg/kcal Unable to determine 1077 mg/ 100 kcal 1270 mg/100 kcal
Fat 5 to 7·5 g/ 100 kcal (except in 3·27 g/100 kcal 6·3 g/100 kcal 5·5 g/100 kcal
cases of hyperlipidaemia)
Fat 2·0 to 3·5 g/100 kcal (when
hyperlipidaemia)
*This composition is typical of most human liquid convalescent diets, and therefore, it recommended that whey protein isolate be added to the formulation after 2-3 days of use
†For smaller gauge tubes, increased volumes of water will be needed to be able to flush through feeding tubes

Journal of Small Animal Practice • Vol 56 • January 2015 • © 2015 British Small Animal Veterinary Association 35
 C. Mansfield & T. Beths

then there should be treatment with antimicrobials for as long as A proportion of humans following AP will have exocrine
possible prior to surgical debridement (Nathens 2004, Johnson insufficiency that is manifested as steatorrhoea and diarrhoea
2005, Heinrich et al. 2006, Muddana et al. 2009) (LOE humans (Wu & Conwell 2010b). One study has shown that the degree
A, dogs B). Surgery to treat pancreatic acute fluid collections in of exocrine insufficiency following a bout of AP in humans is
dogs invariably results in a high mortality rate (>50%), regardless directly correlated with the amount of necrosis (Boreham &
of the technique used (Salisbury et al. 1988, Bellenger et al. 1989, Ammori 2003). Subclinical exocrine pancreatic insufficiency has
Edwards et al. 1990, Johnson & Mann 2006). There have been been diagnosed in dogs and is not always manifested by overt
reported spontaneous resolutions of acute fluid collections in the steatorrhoea (Wiberg & Westermarck 2002). On the basis of
veterinary literature, and good responses to percutaneous drain- this, in severely affected dogs, treatment with exocrine pancreatic
age, suggesting that these are preferable methods for managing enzymes for 3 to 4 weeks following a bout of AP may be benefi-
this particular complication (Smith & Biller 1998, VanEnkevort cial in selected instances (LOE D).
et al. 1999). The authors recommend that the presence of fluid
collections be determined whether a dog has persistent or unex-
CONCLUSION
pected pain, and to perform percutaneous drainage if the pain is
associated with the fluid (LOE humans A, dogs C).
Large, multicentre studies are required to fully evaluate treatment
strategies for AP in dogs. Currently, there exists a reasonable LOE
NOVEL THERAPEUTIC DIRECTIONS for supportive care such as iv fluid therapy and anti-emetic ther-
apy. The areas that seem to hold the most promise for improving
There have been many attempts over the past three decades to morbidity and/or mortality include evaluating novel analgesic
assess new medical treatments for AP. Initially, there was some agents, nutritional intervention and the use of low-dose cortico-
promise for protease inhibitors in either reducing mortality or steroids. Currently, recommendations for analgesia are extrapo-
complications in animal experimental models (Mikami et al. lated from postsurgical studies and are dependent on the level
2005). Stringent analysis of multiple randomised and well- of pain. Extrapolation from humans would suggest that early
controlled clinical trials of protease inhibitors such as gabexate enteral nutrition in dogs with severe AP may decrease morbidity
mesilate in humans have subsequently shown no benefit in any and pain (Petrov et al. 2012, Mirtallo et al. 2012), and it has been
of these agents to reduce mortality or morbidity of AP (Imrie shown that oesophageal feeding is well tolerated in dogs with AP
et al. 1978, Uhl et al. 1999, Heinrich et al. 2006). There was no (Mansfield et al. 2011). There is no evidence to support surgical
amelioration of histological inflammation in a study of dogs with intervention in the management of AP.
induced pancreatitis treated with a somatostatin analogue (Ko Conflict of interest
et al. 1992). Additionally, somatostatin analogues have powerful
None of the authors of this article has a financial or personal
splanchnic vasoconstrictive properties, which may contribute to
relationship with other people or organisations that could inap-
and perpetuate pancreatic necrosis (Klar et al. 1991). The effects
propriately influence or bias the content of the paper.
of specific anti-cytokine therapies appear to be highly variable,
as they are generally useful at ameliorating only one aspect of
References
the inflammatory cascade and require very early administration Al Mofleh, I. (2008) Severe acute pancreatitis: pathogenic aspects and prognostic
(Formela et al. 1994, Imamura et al. 1998, Buscaglia et al. 2008, factors. World Journal of Gastroenterology 14, 675-684
Artinian, V., Krayem, H. & DiGiovine, B. (2006) Effects of early enteral feeding
Pezzilli 2009). The lack of perceived benefit in humans, the lack on the outcome of critically ill mechanically ventilated medical patients. Chest
of widespread availability of veterinary anti-cytokine drugs and 129, 960-996
Bang, U. C., Semb, S., Nojgaard, C. et al. (2008) Pharmacological approach to
prohibitive costs means that these novel therapeutic directions are acute pancreatitis. World Journal of Gastroenterol 14, 2968-2976
unlikely to change management of canine AP in the near future. Bellenger, C. R., Ilkiw, J. E. & Malik, R. (1989) Cystogastrostomy in the treat-
ment of pancreatic pseudocyst/abscess in two dogs. Veterinary Record 125,
181-184
Benchaoui, H. A. (2007) Efficacy of maropitant for preventing vomiting associated
with motion sickness in dogs. Veterinary Record 161, 444-447
FOLLOW-UP CARE Bersenas, A. M., Mathews, K. A., Allen, D. G., et al. (2005) Effects of ranitidine,
famotidine, pantoprazole, and omeprazole on intragastric pH in dogs. American
Journal of Veterinary Research 66, 425-431
Although in most instances, the initiating cause of AP is not Berti, M., Baciarello, M., Troglio, R., et al. (2009) Clinical uses of low-dose ket-
known, in a certain percentage of dogs there may be an under- amine in patients undergoing surgery. Current Drug Targets 10, 707-715
Besselink, M. G., Van Santvoort, H. C., Buskens, E., et al. (2008) Probiotic pro-
lying lipid disorder and therefore it may be prudent to check phylaxis in predicted severe acute pancreatitis: a randomised, double-blind,
fasting serum triglyceride and cholesterol concentrations 1 to placebo-controlled trial. Lancet 371, 651-659
Bhatia, M., Brady, M., Shokuhi, S., et al. (2000) Inflammatory mediators in acute
2 weeks after recovery (Hess et al. 1998). Investigation of under- pancreatitis. Journal of Pathology 190, 117-125
lying causes and long-term management of the hyperlipidaemia Bhoomagoud, M., Jung, T., Atladottir, J., et al. (2009) Reducing extracellular pH
sensitizes the acinar cell to secretagogue-induced pancreatitis responses in
is recommended if present (LOE D). If drug administration is rats. Gastoenterology 137, 1083-1092
implicated in the aetiology, such as azathioprine and potassium Boreham, B. & Ammori, B. J. (2003). A prospective evaluation of pancreatic exo-
crine function in patients with acute pancreatitis: correlation with extent of
bromide, then withdrawal of that drug should be undertaken. necrosis and pancreatic endocrine insufficiency. Pancreatology 3, 303-308
There is no evidence that dogs with dietary indiscretion will Buscaglia, J. M., Simons, B. W., Prosser, B. J., et al. Etanercept: a TNF-alpha bind-
ing agent, is ineffective in the prevention of post-ERCP pancreatitis in canines.
be predisposed to recurrent bouts of AP (Lem et al. 2008). Journal of the Pancreas 9, 456-467

36 Journal of Small Animal Practice • Vol 56 • January 2015 • © 2015 British Small Animal Veterinary Association
 Treatment of acute pancreatitis

Cai, J., Zhou, J., Luo, H. S., et al. (2007) Effect of proton pump inhibitor on amylase acute pancreatitis: 70 cases (1986-1995). Journal of the American Veterinary
release from isolated pancreatic acinie. In Vitro Cellular and Developmental Medical Association 213, 665-670
Biology - Animal 43, 25-27 Hollmann, M. W., Gross, A., Jelacin, N., et al. (2001) Local anesthetic effects on
Cassuto, J., Sinclair, R. & Bonderovic, M. (2006) Anti-inflammatory properties of priming and activation of human neutrophils. Anesthesiology 95, 113-122
local anesthetics and their present and potential clinical implications. Acta Holm, J. L., Chan, D. L. & Rozanski, E. A. (2003) Acute pancreatitis in dogs.
Anaesthesiologica Scandinavica 50, 265-282 Journal of Veterinary Emergency and Critical Care 13, 201-213
Charles, J. (2007) Pancreas. In: Jubb, Kennedy, and Palmer’s Pathology of Holton, L., Pawson, P., Nolan, A., et al. (2001) Development of a behaviour-based
Domestic Animals. vol. 2. Ed M. G. Maxie. Saunders Elsevier, Edinburgh, scale to measure acute pain in dogs. Veterinary Record 148, 525-531
Scotland. pp 389-423 Imamura, M., Mikami, Y., Takahashi, H., et al. (1998) Effect of a specific synthetic
Chebli, J. M. F., Gaburri, P. D., De Souza, A. F. M., et al. (2005) Oral refeeding in inhibitor of neutrophil elastase (ONO-5046) on the course of acute hemor-
patients with mild acute pancreatitis: prevalnce and risk factors of relapsing rhagic pancreatitis in dogs. Journal of Hepatobiliary Pancreatic Surgery 5,
abdominal pain. Journal of Gastroenterology and Hepatology 20, 1385-1389 422-428
Conder, G. A. (2008) Efficacy and safety of maropitant, a selective neurokinin1 Imrie, C. W., Benjamin, I. S., Ferguson, J. C., et al. (1978) A single-centre, double
receptor antagonist, in two randomized clinical trials for prevention of vomit- blind trial of trasylol therapy in primary acute pancreatitis. British Journal of
ing due to motion sickness in dogs. Journal of Veterinary Pharmacology and Surgery 65, 337-340
Therapeutics 31, 528-532 Ioannidis, O., Lavrentieva, A. & Botsios, D. (2008) Nutrition support in acute pan-
Cook, A. K., Breitschwerdt, E. B., Levine, J. F., et al. (1993) Risk factors asso- creatitis. Journal of the Pancreas 9, 375-390
ciated with acute pancreatitis in dogs: 101 cases (1985-1990). Journal of Iovanna, J., Orelle, B., Keim, V., et al. (1991) Messenger RNA sequence and
the American Veterinary Medical Association 203, 673-679 expression of rat pancreatitis-associated protein, a lectin-related protein
De la Puente-Redondo, V. A., Siedek, E. M., Benchaoui, H. A. et al. (2007a) The overexpressed during acute experimental pancreatitis. Journal of Biological
anti-emetic efficacy of maropitant (Cerenia™) in the treatment of ongoing eme- Chemistry 266, 24664-24669
sis caused by a wide range of underlying clinical aetiologies in canine patients Jaffe, R. A. & Rowe, M. A. (1995) Subanesthetic concentrations of lidocaine selec-
in Europe. Journal of Small Animal Practice 48, 93-98 tively inhibit a nociceptive response in the isolated rat spinal cord. Pain 60,
De la Puente-Redondo, V. A., Tilt, N., Rowan, T. G., et al. (2007b) Efficacy of maropi- 167-174
tant for treatment and prevention of emesis caused by intravenous infusion of James, F. E., Mansfield, C. S., Stiener, J. M., et al. (2009) Pancreatic response
cisplatin in dogs. Americal Journal of Veterinary Research 68, 48-56 in healthy dogs fed diets of various fat compositions. American Journal of
Devor, M., Wall, P. D. & Catalan, N. (1992) Systemic lidocaine silences ectopic neu- Veterinary Research 70, 614-618
roma and DRG discharge without blocking nerve conduction. Pain 48, 261-268 Johnson, C. D. (2005) UK Working Party on Acute Pancreatitis: UK guidelines for
Dobromylskyj, P., Flecknell, P. A., Lascelles, B. D., et al. (2000) Pain assessment. the management of acute pancreatitis. Gut 54(Suppl III), iii1-iii9
In: Pain Management in Animals. Eds P. Flecknell and A. Waterman-Pearson. Johnson, M. D. & Mann, F. A. (2006) Treatment for pancreatic abscesses via
Saunders W. B., London, UK. pp 53-79 omentalization with abdominal closure versus open peritoneal drainage in
Donaldson, L. A. & Schenck, W. G. (1979) Experimental acute pancreatitis: the dogs: 15 cases (1994-2004). Journal of the American Veterinary Medical
changes in pancreatic oxygen consumption and the effect of Dextran 40. Association 228, 397-402
Annals of Surgery 190, 728-731 Kalli, I., Adamama-Moraitou, K. K. & Rallis, T. S. (2009) Acute pancreatitis in dogs:
Eatock, F. C., Chong, P., Menezes, N., et al. (2005) A randomized study of early a review article. European J of Companion Animal Practice 19, 147-155
nasogastric versus nasojejunal feeding in severe acute pancreatitis. American Kandil, E., Lin, Y.-Y., Bluth, M. H., et al. (2006) Dexamethasone mediates pro-
Journal of Gastroenterology 100: 432-439 tection against acute pancreatitis via upregulation of pancreatitis-associated
Edwards, D. F., Bauer, M. S., Walker, M. A., et al. (1990) Pancreatic masses in proteins. World Journal of Gastroenterology 12, 6806-6811
seven dogs following acute pancreatitis. Journal of American Animal Hospital Karanjia, N. D., Lutrin, F. J., Chang, Y. B., et al. (1990) Low dose dopamine protects
Association 26, 189-198 against hemorrhagic pancreatitis in cats. The Journal of Surgical Research 48,
Elwood, C., Devauchelle, P., Elliot, J., et al. (2010) Emesis in dogs: a review. Journal 440-443
of Small Animal Practice 51(1): 4-22 Kazantsev, G. B., Hecht, D. W., Rao, R., et al. (1994) Plasmid labeling confirms
Field, B. E., Hepner, G. W., Shabot, M. M., et al. (1979) Nasogastric suction in bacterial translocation in pancreatitis. The American Journal of Surgery 167,
alcoholic pancreatitis. Digestive Diseases and Sciences 24, 339-344 201-207
Firth, A. M. & Haldane, S. L. (1999) Development of a scale to evaluate postop- Keck, T., Friebe, V., Warshaw, A. L., et al. (2005) Pancreatic proteases in serum
erative pain in dogs. Journal of the American Veterinary Medical Association induce leukocyte-endothelial adhesion and pancreatic microcirculatory failure.
214, 651-659 Pancreatology 5, 241-250
Fittschon, C. & Bellamy, J. E. C. (1984) Prednisone treatment alters the serum Kellum, J. A. (2002) Fluid resuscitation and hyperchloremic acidosis in experimen-
amylase and lipase activities in normal dogs and cats without causing pancre- tal sepsis: improved short-term survival and acid-base balance with Hextend
atitis. Canadian Journal of Comparative Medicine 48, 136-140 compared with saline. Critical Care Medicine 30, 300-305
Flint, R. S. & Windsor, J. A. (2003) The role of the intestine in the pathophysi- Kerr, C. (2007). Pain Management 1: systemic analgesics. In: BSAVA Manual of
ology and management of severe acute pancreatitis. World Journal of Canine and Feline Anaesthesia and Analgesia. Eds C. Seymour and T. Duke-
Gastroenterology 5, 69-85 Novakosvski. BSAVA, Quedgeley, UK. pp 89-103
Formela, L. J., Wood, L. M., Whittaker, M., et al. (1994) Amelioration of experimen- King, B. K. & Kudsk, K. A. (1997) A temporal study of TPN-induced changes in gut-
tal acute pancreatitis with a potent platelet-activating factor antagonist. British associated lymphoid tissue and mucosal immunity. Archives of Surgery 132:
Journal of Surgery 81, 1783-1785 1303-1309
Fritz, S., Hackert, T., Hartwig, W., et al. (2010) Bacterial translocation and infected Klar, E., Rattner, D. W., Compton, C., et al. (1991) Adverse effect of therapeutic
pancreatic necrosis in acute necrotizing pancreatitis derives from small bowel vasoconstrictors in experimental acute pancreatitis. Annals of Surgery 214,
rather than from colon. American Journal of Surgery 200, 111-117 168-174
Frossard, J. L. (1999). Gastroenterology 116, 694-701 Knol, J. A., Edgcomb, L. P., Inman, M.G., et al. (1983) Low molecular weight dextran
Frossard, J.-L. & Pastor, C. M. (2002) Experimental acute pancreatitis: new in experimental pancreatitis: effects on pancreatic microcirculation. The Journal
insights into the pathophyisology. Frontiers in Bioscience 7, d275-d287 of Surgical Research 35, 73-82
Fukuyama, K., Iwakiri, R., Noda, T., et al. (2001) Apoptosis induced by ischemia- Ko, T. C., Bertram, M. F., Prinz, R. A., et al. (1992) Effect of somatostatin analogue
reperfusion and fasting in gastric mucosa compared to small intestinal mucosa and cholecystokinin receptor antagonist on bile-induced acute canine pancre-
in rats. Digestive Diseases and Sciences 46, 545-549 atitis. American Journal of Surgery 58, 213-219
Fuller, R. K., Loveland, J. P. & Frankel, M. H. (1981) An evaluation of the efficacy Kotani, J., Usami, M., Nomura, H., et al. (1999) Enteral nutrition prevents bacterial
of nasogastric suction treatment in alcoholic pancreatitis. American Journal of translocation but does not improve survival during acute pancreatitis. Archives
Gastroenterology 75, 349-353 of Surgery 134, 287-292
Gardner, T. B., Vege, S. S., Pearson, R.K., et al. (2008) Fluid resuscitation in acute KuKanich, B. & Papich, M. G. (2004) Pharmacokinetics of tramadol and
pancreatitis. Clinical Gastroenterology and Hepatology 6, 1070-1076 the metabolite O-desmethyltramadol in dogs. J Vet Pharmacol Ther 27(4):
Gaynor, J. S. (2008) Control of cancer pain in veterinary patients. Veterinary Clinics 239-246
of North America: Small Animal Practice 38, 1429-1448, viii Kumar, A., Singh, N., Prakash, S., et al. (2006) Early enteral nutrition in severe
Hackert, T., Tudor, S., Felix, K., et al. (2010) Effects of pantoprazole in experimen- acute pancreatitis: a prospective randomized controlled trial comparing nasoje-
tal acute pancreatitis. Life Sciences 87, 551-557 junal and nasogastric routes. J Clin Gastroenterol 40(5): 431-434
Heinrich, S., Schafer, M., Roussan, V., et al. (2006) Evidence-based treatment of Lamont, L. A. (2008) Adjunctive analgesic therapy in veterinary medicine.
acute pancreatitis: a look at established paradigms. Annals of Surgery 243, Veterinary Clinics of North America: Small Animal Practice 38(6): 1187-1203
154-168 Lascelles, B. D., Cripps, P. J., Jones, A., Waterman, A. E., et al. (1997) Post-
Heller, A. (1999) Pancreatitis-associated protein protects the lung from leukocyte- operative central hypersensitivity and pain: the pre-emptive value of pethidine
induced injury. Anesthesiology 91, 1408-1414 for ovariohysterectomy. Pain 73(3): 461-471
Hernandez, G., Velasco, N., Wainstein, C., et al. (1999) Gut mucosal atrophy after Lasson, A. & Ohlsson, K. (1984) Protease inhibitors in acute human pancreatitis.
a short enteral fasting period in critically ill patients. Journal of Critical Care Scandinavian Journal of Gastroenterology 19, 779-786
14, 73-77 Leese, T., Holliday, M., Heath, D., et al. (1987) Multicentre clinical trial of low
Hess, R. S., Saunders, H. M., Van Winkle, T. J., et al. (1998) Clinical, clinico- volume fresh frozen plasma therapy in acute pancreatitis. British Journal of
pathologic, radiographic, and ultrasonographic abnormalities in dogs with fatal Surgery 74, 907-911

Journal of Small Animal Practice • Vol 56 • January 2015 • © 2015 British Small Animal Veterinary Association 37
 C. Mansfield & T. Beths

Leese, T., West, K., Morton, D., et al. (1988) Fresh frozen plasma therapy in acute Noble, M. D., Romac, J., Vigna, S. R., et al. (2008) A pH-sensitive, neurogenic
pancreatitis: an experimental study. International J Gastrointestinal Cancer 3, pathway mediates disease severity in a model of post-ERCP pancreatitis. Gut
437-447 57, 1566-1571
Leese, T., Thomas, W. M., Holliday, M., et al. (1991) A multicentre controlled clini- Ortiz, E. M., Dusetti, N. J., Vasseur, S., et al. (1998) The pancreatitis-associated
cal trial of high-volume fresh frozen plasma therapy in prognostically severe protein is induced by free radicals in AR4-2J cells and confers cell resistance to
acute pancreatitis. Annals of the Royal College of Surgeons of England 73, apoptosis. Gastroenterology 114, 808-816
207-214 Pandey, S. K., Ahuja, V., Joshi, Y. K., et al. (2004) A randomized trial of oral refeed-
Leffler, A. (2009) Characterization of species-related differences in the pharmacol- ing compared with jejunal tube refeeding in acute pancreatitis. Indian Journal of
ogy of tachykinin NK receptors 1, 2 and 3. Biochemical Pharmacology 77, 1522 Gastroenterology 23, 53-55
Lem, K. Y., Fosgate, G.T., Norby, B., et al. 2008, Associations between dietary Parent, J. (1982) Effects of dexamethasone on pancreatic tissue and on serum
factors and pancreatitis in dogs. Journal of the American Veterinary Medical amylase and lipase activities in dogs. Journal of the American Veterinary
Association 233, 1425-1431 Medical Association 180, 743-746
Lemke, K. A. & Creighton, C. M. (2010) Analgesia for anesthetized patients. Pastor, C. M. & Frossard, J.-L. (2001) Are genetically modified mice useful for the
Topics in Companion Animal Medicine 25, 70-82 understanding of acute pancreatitis. FASEB Journal 15, 893-897
Levant, J. A., Secrist, D. M., Resin, H., et al. (1974) Nasogastric suction in the Pearce, C. B., Sadek, S. A., Walters, A. M., et al. (2006) A double-blind, ran-
treatment of alcoholic pancreatitis: a randomised study. Journal of the American domised, controlled trial to study the effects of an enteral feed supplemented
Medical Association 229, 51-52 with glutamine, arginine, and omega-3 fatty acid in predicted acute severe pan-
Loiudice, T. A., Lang, J., Mehta, H., et al. (1984) Treatment of acute alcoholic pan- creatitis. Journal of the Pancreas 7, 361-371
creatitis: the roles of cimetidine and nasogastric suction. American Journal of Peng, Y.-S., Wu, C.-S., Chen, Y-C., et al. (2009) Critical illness-related corticoste-
Gastroenterology 79, 553-558 roid insufficiency in patients with severe acute biliary pancreatitis: a prospec-
Manas, M., Yago, M. D., Quiles, J. L., et al. (1996) Absence of rapid adaptation tive cohort study. Critical Care 13, R123.
of the exocrine pancreas of conscious dogs to diets enriched in fat or carbohy- Petrov, M. S. & Zagainov, V. E. (2007) Influence of enteral versus parenteral nutri-
drates. Archives of Physiology Biochemistry 104, 819-825 tion on blood glucose control in acute pancreatitis: a systematic review. Clinical
Mansfield, C. S. (2012) Pathophysiology of acute pancreatitis: potential appli- Nutrition 26, 514-523
cation from experimental models and human medicine to dogs. Journal of Petrov, M. S., Correia, M. I. T. D. & Windsor, J. A. (2008) Nasogastric tube feeding
Veterinary Internal Medicine 26, 875-887 in predicted severe acute pancreatitis. A systematic review of the literature to
Mansfield, C. S., James, F. E. & Robertson, I. D. (2008) Development of a clini- determine safety and tolerance. Journal of the Pancreas 9, 440-448
cal severity index for dogs with acute pancreatitis. Journal of the American Petrov, M. S., McIlroy, K., Grayson, L., et al. (2012) Early nasogastric tube feeding
Veterinary Medical Association 233, 936-944 versus nil per os in mild to moderate acute pancreatitis: a randomized con-
Mansfield, C. S., James, F. E., Steiner, J., et al. (2011) A pilot study to assess tol- trolled trial. Clinical Nutrition 32, 697-703
erability of early enteral nutrition via esophagostomy tube feeding in dogs with Pezzilli, R. (2009) Pharmacotherapy for acute pancreatitis. Expert Opinion on
severe acute pancreatitis. Journal of Veterinary Internal Medicine 25, 419-425 Pharmacotherapy 10, 2999-3014
Marik, P. E. (2008) Recommendations for the diagnosis and management of corti- Powell, J. J., Murchison, J. T., Fearon, K. C., et al. (2000) Randomized controlled
costeroid insufficiency in critically ill adult patients: consensus statements from trial of the effect of early enteral nutrition on markers of the inflammatory
an international task force by the American College of Critical Care Medicine. response in predicted severe acute pancreatitis. British Journal of Surgery
Critical Care Medicine 36, 1937-1949 87(10): 1375-1381
Marik, P. & Pinsky, M. (2003) Death by total parenteral nutrition. Intensive Care Price, J. & Nolan, A. M. (2007) The physiology and pathophysiology of pain. BSAVA
Medicinee 29, 867-869 Manual of Canine and Feline Anaesthesia and Analgesia. Eds C. Seymour and
Mastrocinque, S. & Fantoni, D. T. (2003) A comparison of preoperative tramadol T. Duke-Novakoski. BSAVA, Quedgeley, UK. 79-88.
and morphine for the control of early postoperative pain in canine ovariohyster- Pupelis, G., Selga, G., Austrums, E., et al. (2001) Jejunal feeding, even when
ectomy. Veterinary Anaesthesia and Analgesia 30, 220-228 instituted late, improves outcomes in patients with severe pancreatitis and
Mathews, K. A. (2000) Pain assessment and general approach to management. peritonitis. Nutrition 17, 91-94
Veterinary Clinics of North America: Small Animal Practice 30(4): 729-755, v. Qin, H. L., Su, Z. D., Gao, Q., et al. (2002a) Early intrajejunal nutrition: bacte-
Mehler, S. J., Mayhew, P. D., Drobatz, K. J., et al. (2004) Variables associated rial translocation and gut barrier function of severe acute pancreatitis in dogs.
with outcome in dogs undergoing extrahepatic biliary surgery: 60 cases (1988- Hepatobiliary Pancreatic Diseases International 1, 150-154
2002). Veterinary Surgery 33, 644-649 Qin, H. L., Su, Z. D, Hu, L.G., et al. (2002b) Effect of early intrajejunal nutrition
Mikami, Y., Takeda, K., Matsuda, K., et al. (2005) Rat experimental model of con- on pancreatic pathological features and gut barrier function in dogs with acute
tinuous regional arterial infusion of protease inhibitor and its effects on severe pancreatitis. Clinical Nutrition 21, 469-473
acute pancreatitis. Pancreas 30, 248-253 Qin, H. L., Su, Z. D., Hu, L. G., et al. (2003) Parenteral versus early intrajejunal
Mirtallo, J. M. (2012) International consensus guidelines for nutrition therapy in nutrition: effect on pancreatitic natural course, entero-hormones release and
pancreatitis. Journal of Parenteral and Enteral Nutrition 36, 284-291 its efficacy on dogs with acute pancreatitis. World Journal of Gastroenterology
Mithofer, K., Warshaw, A. L., Frick, T. W., et al. (1995) Calcium administration 9, 2270-2273
augments pancreatic injury and ectopic trypsinogen activation after temporary Qin, H. L., Su, Z. D., Hu, L. G., et al. (2007) Effect of parenteral and early intrajeju-
systemic hypotension in rats. Anesthesiology 83, 1266-1273 nal nutrition on pancreatic digestive enzyme synthesis, storage and discharge
Mohr, A. J., Leisewitz, A. L., Jacobson, L. S., et al. (2003) Effect of early enteral in dog models of acute pancreatitis. World Journal of Gastroenterology 13,
nutrition on intestinal permability, intestinal protein loss, and outcome in dogs 1123-1128
with severe parvoviral enteritis. Journal of Veterinary Internal Medicine 17, Queau, Y., Larsen, J. A., Kass, P. H., et al. (2011) Factors associated with adverse
791-798 outcomes during parenteral nutrition administration in dogs and cats. Journal
Morton, C. M., Reid, J., Scott, E. M, et al. (2005) Application of a scaling model to of Veterinary Internal Medicine 25, 446-452
establish and validate an interval level pain scale for assessment of acute pain Rau, S. E., Barber, L. G. & Burgess, K. E. (2010) Efficacy of maropitant in the
in dogs. American Journal of Veterinary Researh 66, 2154-2166 prevention of delayed vomiting associated with administration of doxorubicin to
Muddana, V., Whitcomb, D. C. & Papachristou, G. I. (2009) Current Management dogs. Journal of Veterinary Internal Medicine 24, 1452-1457
and novel insights in acute pancreatitis. Expert Review of Gastroenterology and Reuter, J. D., Marks, S.L., Rogers, Q. R., et al. (1998) Use of total parenteral
Hepatology 3, 435-444 nutrition in dogs: 209 cases (1988-1995) Journal of Veterinary Emergency and
Muller, C. A., Vogeser, M., Belyaev, O., et al. (2006) Role of endogenous gluco- Critical Care 8, 201-213
corticoid metabolism in human acute pancreatitis. Critical Care Medicine 34, Rinderknecht, H. (1986) Activation of pancreatic zymogens: normal activation, pre-
1060-1066 mature intrapancreatic activation, protective mechansims against inappropriate
Murrell, J. C., Psatha, E. P., Scott, E. M., et al. (2008) Application of a modified form activation. Digestive diseases and Sciences 31, 314-321
of the Glasgow pain scale in a veterinary teaching centre in the Netherlands. Saker, K. E. & Remillard, R. L. (2010) Critical care nutrition and enteral-assisted
Veterinary Record 162, 403-408 feeding. In: Small Animal Clinical Nutrition. Eds M. S. Hand, M. S. Thatcher and
Naeije, R., Salingret, E., Clumeck, N., et al. (1978) Is nasogastric suction neces- R. L. Remillard. 5th ed. Mark Morris Institute, Topeka, KS, USA. pp 439-476
sary in acute pancreatitis? British Journal of Medicine 2, 659-660 Salisbury, S. K., Lantz, G. C., Nelson, R.W., et al. (1988) Pancreatic abscess
Nathens, A. B. (2004) Management of the critically ill patient with severe acute in dogs: six cases (1978-1986) Journal of American Veterinary Medical
pancreatitis. Critical Care Medicine 32, 2524-2536 Association 193, 1104-1108
Navarro, S., Roe, E., Aused, R., et al. (1984) Comparison of fasting, nasogastric Sarac, T. P., Souba, W. W., Miller, J. H., et al. (1994) Starvation induces differential
suction and cimetidine in the treatment of acute pancreatitis. Digestion 30, small bowel luminal amino acid transport. Surgery 116, 679-685
224-230 Sarr, M. G., Sanfey, H. & Cameron, J. L. (1986) Prospective, randomized trial of
Newman, S. J., Steiner, J. M., Woosley, K., et al. (2006) Histologic assessment and nasogastric suction in patients with acute pancreatitis. Surgery 100, 500-504
grading of the exocrine pancreas in the dog. Journal of Veterinary Diagnostic Schmidt, J., Fernandez-del-Castillo, C., Rattner, D. W., et al. (1993) Hyperoncotic
Investigation 18, 115-118 ultrahigh molecular weight dextran solutions reduce trypsinogen activation, pre-
Niederau, C., Niederau, M., Luthen, R., et al. (1990) Pancreatic exocrine secretion vent acinar necrosis, and lower mortality in rodent pancreatitis. The American
in acute experimental pancreatitis. Gastroenterology 99, 1120-1127 Journal of Surgery 165, 40-45

38 Journal of Small Animal Practice • Vol 56 • January 2015 • © 2015 British Small Animal Veterinary Association
 Treatment of acute pancreatitis

Schmidt, J., Huch, K., Mithofer, K., et al. (1996) Benefits of various dextrans after Vigneault, L., Turgeon, A. F., Cote, D., et al. (2011) Perioperative intravenous lido-
delayed therapy in necrotizing pancreatitis of the rat. Intensive Care Medicine caine infusion for postoperative pain control: a meta-analysis of randomized
22, 1207-1213 controlled trials. Canadian Journal of Anesthesia 58, 22-37
Sedlacek, H. S., Ramsey, D. S, Boucher, J. F., et al. (2008) Comparative efficacy Wagner, A. E., Walton, J. A. & Hellyer, P. W., et al. (2002) Use of low doses of
of maropitant and selected drugs in preventing emesis induced by centrally or ketamine administered by constant rate infusion as an adjunct for postopera-
peripherally acting emetogens in dogs. Journal of Veterinary Pharmacology and tive analgesia in dogs. Journal of the American Veterinar y Medical Association
Therapeutics 31, 533-537 221, 72-75
Smith, S. A. & Biller, D. S. (1998) Resolution of a pancreatic pseudocyst in a Watson, P. (2004) Pancreatitis in the dog: dealing with a spectrum of disease. In
dog following percutaneous ultrasonographic-guided drainage. Journal of the Practice 26, 64-77
American Animal Hospital Association 34, 515-522 Watson, P. J., Roulois, A. J., Scase, T., et al. (2007) Prevalence and breed distribu-
Souba, W. W., Klimberg, V. S., Plumley, D. A., et al. (1990) The role of glutamine in tion of chronic pancreatitis at post-mortem examination in first-opinion dogs.
maintaining a helathy gut and supporting the metabolic response to injury and Journal of Small Animal Practice 48, 609-618
infection. Journal of Surgical Research 48, 383-391 Weatherton, L. K. & Streeter, E. M. (2009) Evaluation of fresh frozen plasma
Stevens, T., Conwell, D. L. & Zuccaro, G. (2004) Pathogenesis of chronic pan- administration in dogs with pancreatitis: 77 cases (1995-2005). Journal of
creatitis: an evidence-bsed review of past theories and recent developments. Veterinary Emergency and Critical Care (San Antonio) 19, 617-622
American Journal of Gastroenterology 99, 2256-2270 Williams, D. A. (1994) Diagnosis and management of pancreatitis. Journal of
Stewart, A. F. (1994) Pancreatitis in dogs and cats: cause, pathogenesis, diag- Small Animal Practice 35, 445-454
nosis, and treatment. Compendium on Continuing Education for the Practising Windsor, J. A. & Hammodat, H. (2000) Metabolic management of severe acute
Veterinarian 16, 1423-1430 pancreatitis. World Journal of Surgery 24, 644-672
Strombeck, D. R. (1990) The exocrine pancreas. In: Small Animal Gastroenterology. Wu, B. U. & Conwell, D. L. (2010a) Acute pancreatitis. Part I: Approach to early
D. R. Strombeck and W. G. Guilford. Stonegate Publishing, Davis, CA, USA. management. Clinical Gastroenterology and Hepatology 8, 410-416
p 429 Wu, B. U. & Conwell, D. L. (2010b) Acute pancreatitis. Part II: approach to follow-
Sun, W., Watanabe, Y., Toki, A., et al. (2007) Beneficial effects of hydrocortisone up.Clinical Gastroenterology and Hepatology 8, 417-422
in induced acute pancreatitis of rats. Chinese Medical Journal (England) 120, Wu, B. U., Hwang, J. Q., Gardner, T. H., et al. (2011) Lactated Ringer’s solution
1757-1761 reduces systemic inflammation compared with saline in patients with acute
Thomson, A. (2006) Nutrition therapy in acute pancreatitis. Journal of Parenteral pancreatitis. Clinical Gastroenterology and Hepatology 9, 710-717, e711.
and Enteral Nutrition 30, 536-537; author reply 537-538 Zenilman, M. E., Magnuson, T. H., Swinson, K., et al. (1996) Pancreatic thread pro-
Tolbert, K., Bissett, S., King, A., et al. (2011) Efficacy of oral famotidine and 2 tein is mitogenic to pancreatic-derived cells in culture. Gastroenterology 110,
omeprazole formulations for the control of intragastric pH in dogs. Journal of 1208-1214
Veterinary Internal Medicine 25, 47-54 Zhang, L., Zhang, X. & Westlund, K. N. (2004) Restoration of spontaneous explor-
Uhl, W., Buchler, M., Malfertheiner, P., et al. (1999) A randomised, double blind, atory behaviors with an intrathecal NMDA receptor antagonist or a PKC inhibi-
multicentre trial of octreotide in moderate to severe acute pancreatitis. Gut tor in rats with acute pancreatitis. Pharmacology Biochemistry & Behavior 77,
45, 97-104 145-153
VanEnkevort, B. A., O’Brien, R. T., Young, K. M. (1999) Pancreatic pseudocysts in
4 dogs and 2 cats: ultrasonographic and clinicopathologic findings. Journal of
Veterinary Internal Medicine 13, 309-313

Journal of Small Animal Practice • Vol 56 • January 2015 • © 2015 British Small Animal Veterinary Association 39