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15 August 2019

Canine pancreatitis – Current


thoughts on diagnosis and
treatment

Darren Merrett
BVSc (Hons) CertSAC MVS FANZCVS
29/07/2019

Acute Canine
Pancreatitis
Why talk about acute
Darren Merrett pancreatitis?
BVSc (Hons) CertSAC MVS FANZCVS

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Pancreatitis = clinical challenge What are we going to talk about?


• Relatively common • What goes wrong? (pathophysiology)
• Widely differing clinical entities from mild and transient to lethal • Why do things go wrong? (aetiology)
• Loads of differentials for the non-specific presentation • Who gets it? (signalment)
• Lots of diagnostic tests (a bad sign) with no gold standard • What signs do they show?
• No specific treatment • How do we tell what is going wrong? (diagnosis)
• What do we do about it? (treatment)

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Normal Pancreas
• Potent digestive enzymes secreted and stored in
granules as inactive zymogens OR active enzymes
but lacking co-factor
• Pancreatic secretory trypsin inhibitor (PSTI) inhibits

Pathophysiology any trace amounts of trypsin that may be produced


• Zymogen granules are physically separated from
lysosomal granules as part of the safeguards that
govern lysosome function
• Circulating protease inhibitors will mop up any
activated enzymes that enter the circulation
JVIM 2012; 26: 875-887

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Normal Pancreas
Pancreatic secretory trypsin inhibitor = SERINE PROTEASE INHIBITOR,
KAZAL-TYPE, 1

PSTI = SPINK1

https://veteriankey.com/pancreas-2/

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Normal Pancreas Pathophysiology of Pancreatitis


• Trypsinogen is activated to trypsin within the acinar cell
• Secretion from the acinar cell to the pancreatic duct is inhibited
• Zymogen granules and lysosomal granules come together
• Further activation of trypsin and all the other digestive enzymes
• PSTI (SPINK1) is overwhelmed
• Activated enzymes spill into the interstitium

https://courses.washington.edu/conj/bess/zymogens/zymogens.html

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Pathophysiology of Pancreatitis Pathophysiology of Pancreatitis


• Trypsinogen is activated to trypsin within the acinar cell • Trypsinogen is activated to trypsin
• Secretion from the acinar cell is blocked (although synthesis
• Cause is unknown???? Theories about disorders of: continues)
• Trypsinogen
• Trypsinogen gene mutations associated with hereditary pancreatitis in people
• PSTI (SPINK1)
• Cathepsin B (lysosomal protease)
• Calcium regulation
• pH regulation

JVIM 2012; 26: 875-887

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Pathophysiology of Pancreatitis Pathophysiology of Pancreatitis


• Trypsinogen is activated to trypsin • INAPPROPRIATE ENZYME ACTIVATION 
• Secretion from the acinar cell to the pancreatic duct is blocked • Local Effects
• If sufficiently severe inflammatory stimulus will trigger systemic inflammation
• Dysregulation within acinar cell  further activation of trypsinogen
AND other digestive enzymes

INAPPROPRIATE ENZYME ACTIVATION

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Pathophysiology of Pancreatitis Pathophysiology of Pancreatitis


• Local Effects • Inflammation
• Microcirculatory injury • Normally there is a balance of pro and anti inflammatory mediators that will
• Leukocyte chemoattraction and release of cytokines institute and maintain inflammation as required BUT turn it off when danger
• Oxidate stress has passed
• Severe inflammation can trigger a failure of homeostasis with subsequent
systemic inflammatory response syndrome (SIRS) what will lead to multiple
• Damage to vascular endothelium, interstitium and acinar cells which will organ failure syndrome (MODS)
exacerbate the pathology

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J Vet Intern Med 2012;26:457–482 J Vet Intern Med 2012;26:457–482

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Pathophysiology of Pancreatitis Pathophysiology of Pancreatitis


• As a consequence widespread distant effects but gut is important • INAPPROPRIATE ENZYME ACTIVATION 
• Susceptible to ischaemia • Local Effects
• Increased intestinal permeability  bacterial and inflammatory cell • If sufficiently severe inflammatory stimulus will trigger systemic inflammation
translocation

• Do bacteria have a role? One study in cats using FISH found:


• 13/46 cats with pancreatitis had bacterial colonisation of glandular tissue, fat,
connective tissue, within ducts, areas of necrosis
• 11/31 with moderate to severe pancreatitis
• 2/15 with mild pancreatitis

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Aetiology and Associations


• Most cases are IDIOPATHIC

Aetiology and Associations

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Aetiology and Associations Aetiology and Associations


• Hypercalcaemia
• High fat (low protein) diets • Very rare
• Experimentally induced pancreatitis
• Drugs – LOTS associated but proof??
• BUT lots of working and sled dogs are fed on high fat diets without obvious • Potassium bromide
harm • Several chemotherapy agents e.g. L-asparaginase, vinca alkaloids, cisplatin
• Frusemide
• Maybe triglycerides are more important • Azathioprine
• Thiazide diuretics
• Miniature schanuzers are prone
• Sulphonamides
• Infuse pancreas ex vivo with triglycerides  rapid oedema and haemorrhage • Tetracyclines
• Associated with diseases that cause hypertriglyceridaemia: DM, HAC, hypoT • Cholinesterase inhibitor insecticides
• Zinc
• NOT CORTICOSTEROIDS

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Aetiology and Associations Aetiology and Associations


• Pancreatic duct obstruction? • Autoimmune - ?English Cocker spaniels
• Duodenal reflux? • In UK population of English Cocker spaniels with CHRONIC pancreatitis that
differs from other breeds
• Trauma including surgical • Fibrosis is interlobular and periductular
• Ischaemia, hypotension • Loss of ducts
• Inflamm is predominantly T cell
• Infectious • In particular the loss of ducts and T cell rich inflammation is similar to the
• Babesia, Leishmania, Toxoplasma, liver flukes appearance of auto-immune pancreatitis in humans
• Complication of renal failure and liver disease

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Risk Factors Risk Factors


• Retrospective case-control study
JAVMA 2008;233:1425–1431) • Inappropriate food
• Ingestion of rubbish
• Recent OR life-long feeding of table scraps
• Obesity
• Min schnauzers, York Terr and terriers in general
• Previous surgery
• Other endocrinopathies
• Diabetes mellitus
• Hyperadrenocorticism
JAVMA 1999;214:46-51

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Risk Factors Aetiology Risk Factors


• Inappropriate food • Idiopathic • Inappropriate food
• Ingestion of rubbish • Elevated triglycerides • Obesity
• Recent OR life-long feeding of table scraps • ?Auto-immune (Eng Cocker Span) • Many breeds (Min Schnauzer, terriers,
etc)
• Obesity • Trauma including surgical • Previous surgery
• Min schnauzers, York Terr and terriers in general • Ischaemia, hypotension • Endocrinopathies: DM, HAC, hypoT
• Previous surgery • Epilepsy or its treatment
• Rare causes
• Infectious
• Other breeds variable reported Cocker spaniels, Labradors, Boxers, Border • Complication of renal failure and liver
disease
collies, CKCS, etc…. • Drugs
• Male or neutered female • Hypercalcaemia
• Endocrinopathies: DM, HAC, hypoT • Maybe
• Pancreatic duct obstruction?
• Epilepsy or its treatment • Duodenal reflux?

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Signalment
• Middle aged + (few mths – 15+yr)
• Min schnauzer, Terriers, Cocker spaniels, CKCS,

Clinical Signs and Findings

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Clinical Signs and Findings Clinical Signs and Findings


• NON SPECIFIC • NON SPECIFIC
• Variable severity: mild  fatal • Variable severity: mild  fatal

• Anorexia and lethargy • ACUTE ABDOMEN


• Vomiting
• Abdominal pain
• Diarrhoea
• Dehydration
• Icterus

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Differentials for acute abdomen . . . How many are surgical indications?


• Metabolic: Addison’s disease, • Metabolic: Addison’s disease,
• GIT: gastrointestinal ulceration, foreign body, torsion, intussusception, gastroenteritis, tumour, GDV, • GIT: gastrointestinal ulceration, foreign body, torsion, intussusception, gastroenteritis, tumour, GDV, intestinal
intestinal volvulus, cecal inversion, colitis, obstipation, HGE volvulus, cecal inversion, colitis, obstipation
• Hepatobiliary: hepatitis (toxic, infectious (viral, bacterial, fungal, parasitic, algal)), hepatobiliary • Hepatobiliary: hepatitis (toxic, infectious (viral, bacterial, fungal, parasitic, algal), hepatobiliary neoplasia, liver lobe
neoplasia, liver lobe torsion, hepatic rupture, hepatic abscess, biliary mucocele, cholecystitis, torsion, hepatic rupture, hepatic abscess, biliary mucocele, cholecystitis, cholelithiasis, portosystemic shunt
cholelithiasis, portosystemic shunt
• Urinary: renal torsion, renal abscess, trauma/avulsion/rupture, pyelonephritis, renal or ureteral • Urinary: renal torsion, renal abscess, trauma/avulsion/rupture, pyelonephritis, renal or ureteral urolithiasis,
urolithiasis, prostatitis, prostatic neoplasia, prostatic cyst, prostatic abscess prostatitis, prostatic neoplasia, prostatic cyst, prostatic abscess
• Adrenal: ruptured adrenal tumour causing retroperitoneal haemorrhage • Adrenal: ruptured adrenal tumour causing retroperitoneal haemorrhage
• Spleen: splenic torsion, splenic abscess, splenic tumour • Spleen: splenic torsion, splenic abscess, splenic tumour
• Mesentery and lymph nodes: lymphoma, malignant histiocytosis, mesenteric torsion, mesenteric • Mesentery and lymph nodes: lymphoma, malignant histiocytosis, mesenteric torsion, mesenteric avulsion, adhesions
avulsion, adhesions with organ entrapment, internal hernia with organ entrapment, internal hernia
• Peritoneum: septic (ruptured abdominal abscess, migrating foreign body) or sterile • Peritoneum: septic (ruptured abdominal abscess, migrating foreign body) or sterile (uroperitoneum, bile peritonitis,
(uroperitoneum, bile peritonitis, haemabdomen) peritonitis haemabdomen) peritonitis
• Pancreas: pancreatitis, pancreatic phlegmon, pancreatic abscess, pancreatic tumour • Pancreas: pancreatitis, pancreatic phlegmon, pancreatic abscess, pancreatic tumour
• Reproductive: testicular torsion, orchitis, metritis, pyometra, uterine torsion, ovarian cyst, ovarian • Reproductive: testicular torsion, orchitis, metritis, pyometra, uterine torsion, ovarian cyst, ovarian tumour
tumour • Referred back pain presenting as abdominal pain
• Referred back pain presenting as abdominal pain

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How many are surgical indications? Clinical Signs and Findings


• Acute obstruction
• Intestinal or urinary
• NON SPECIFIC
• Ruptured organ • Variable severity: mild  fatal
• Intestinal perforation
• Torsion • ACUTE ABDOMEN
• Intestine, spleen, liver lobe, uterus, testicle
• GDV
• Biliary mucocoele (mature)
• Vascular occlusion
• Maybe
• Abscess
• Bleeding lesion

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Aim of diagnostics
1. Find evidence to SUPPORT the diagnosis of pancreatitis

2. EXCLUDE alternative diagnoses, particularly SURGICAL INDICATIONS


• Obstruction

Diagnosing Pancreatitis •

Rupture
Torsion
• Perforation
• GDV
• Biliary mucocoele
• Vascular occlusion

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Aim of diagnostics Pancreatic Diagnostics - Difficulties


1. Find evidence to SUPPORT the diagnosis of pancreatitis • Variation in severity

2. EXCLUDE alternative diagnoses, particularly SURGICAL INDICATIONS


• Obstruction • To judge the utility of diagnostic tests we need a gold standard to
• Rupture History
Physical examination
assess efficacy
• Torsion
Imaging
• Perforation
Clinpath There is NO gold standard!
• GDV
Exploratory surgery
• Biliary mucocoele
• Vascular occlusion

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What standards for Dx are used? Histopathology


• In different papers the diagnosis of pancreatitis is achieved 101 dogs post mortem
differently: No record of cause of death
• Histopathological changes only Pancreas sectioned every 2 cm
• Histopathological changes + clinical signs • Hyperplastic nodules 80.2%
• Clinical signs + imaging • Lymphocytic inflammation 52.5%
• Fibrosis 49.5%
• Clinical signs + imaging + clinical pathology
• Atrophy 46.5%
• Clinical signs + clinical pathology
• Neutrophilic inflammation 31.7%
• Fat necrosis 25.7%
• This variance can make assessing efficacy of tests difficult • Pancreatic necrosis 16.8%
• Oedema 9.9%

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Histopathology Histopathology
151 dogs (originally 200 dogs but 49 with autolysis) 73 dogs post mortem
No record of cause of death No record of cause of death
• Chronic pancreatitis 34% • Abnormalities in 64.3% (47/73)
• Acute pancreatitis 2.6% • Suppurative inflammation 32.9%
• Pancreatic neoplasia 3% • Pancreatic necrosis 31.5%
• No abnormalities 22% • Lymphocytic inflammation 46.6%
• Significant fibrosis 23% • Of the 47 dogs with abnormalities 28/47 with fibrosis
• Other changes 16%

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Routine Clinical Pathology Routine Clinical Pathology


• Haemogram – Almost anything!! Variably may see: • Serum biochemistry – Variably may see:
• Anaemia  polycythaemia •  liver enzymes
• Leukocytosis  leukopenia •  bilirubin
• Thrombocytopenia •  urea/creatinine
•  albumin
• electrolyte abnormalities most commonly:  Na, K, Cl, Ca
•  triglycerides/cholesterol
•  or  glucose

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Test Result Test Result Very sensitive test


• Gets most/all of the cases
• BUT includes some normals
so not very specific

Disease Present Disease Absent Disease Present Disease Absent

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Sensitivity Test Result Very specific test


TEST POSITIVE TEST NEGATIVE • Gets very few normals
SICK True Positive False Negative • BUT misses some affected
so not very sensitive
HEALTHY False Positive True Negative

Sensitivity is the proportion of patients who tested positive for the disease
amongst those who are sick

Sensitivity = True Positive


Total number of sick (true positives + false negatives)

A very sensitive test will detect LOTS of the patients that have the problem
Disease Present Disease Absent

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Specificity
TEST POSITIVE TEST NEGATIVE Low specificity
SICK True Positive False Negative High specificity
HEALTHY False Positive True Negative

Specificity is the proportion of patients who tested negative for the disease
amongst those who are healthy
High sensitivity
Specificity = True Negative
Total number of healthy (false positives + true negatives) Low sensitivity

A very specific test will mainly give positive results only in those patients that
have the problem

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Amylase/Lipase Amylase/Lipase

• Traditionally: • In severe cases of pancreatitis


• amylase/lipase elevations have been taken to indicate pancreatic disease
• elevations > 3x support a Dx of pancreatitis Amylase Lipase
• elevations < 3x may occur with pancreatitis, but can also be seen in GIT and
renal disease
Dogs Increased in 69% Increased in 39%

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Amylase/Lipase Amylase/Lipase
• Generally speaking in DOGS . . . • Elevations of amylase/lipase may be seen in:
• Sensitivity for any increase in pancreatitis cases ~30-70% • intestinal disease
• If you apply >3x cut-off sensitivity ~15% • renal disease
• hepatic disease
• prostatic disease
• post abdominal surgery
• Amylase/lipase are not particularly sensitive in the detection of • corticosteroid administration   lipase up to 5x
acute pancreatitis in dogs!
• Amylase/lipase are not particularly specific in the detection of acute
pancreatitis

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Pancreatic lipase Pancreatic lipase


• Pancreas specific • Spec cPL
• Two assays:
• Spec cPL – quantitative
• SNAP cPL – semi-quantitative
Panc Lipase Normal Grey zone Suggestive

DOG <200 ug/L 201 – 399 ug/L ≥ 400 ug/L

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Pancreatic lipase Spec cPL


• SNAP cPL – semi-quantitative • Sensitivity and specificity
• Positive result will occur ‘somewhere’ >200 ug/L • Varies depending on severity of pancreatitis
• Positive result will include equivocal results • Sensitivity 21-88%
• Recommendation is to follow up a +ve with spec cPL • Specificity 81-100%
• Many studies rely on histological diagnosis at post mortem

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Spec cPL Spec cPL


• In the real world • In the real world
• Acute abdomen • Acute abdomen
• 57 with pancreatitis • 11 with pancreatitis
• 27 controls • 27 other (intestinal FB, hepatic or splenic masses, peritonitis)

Acute Abdomen Spec cPL <200 Spec cPL >200 Spec cPL >400
Sensitivity Specificity ug/L ug/L ug/L

Spec cPL >400 ug/L 72-78% 81-88%


Pancreatitis 2/10 8/10 7/8
Spec cPL >200 ug/L 87-94% 66-77% Other 20/26 6/26 6/6

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Spec cPL Spec cPL


• In the real world
• Acute abdomen
• 11 with pancreatitis • In the real world
• 27 other (intestinal FB, hepatic or splenic masses, peritonitis) • 26 dogs with pancreatitis

Sensitivity Specificity Spec cPL <200 ug/L 200-400 ug/L >400 ug/L

Spec cPL 70% 77% Pancreatitis 8/26 4/26 14/26

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Spec cPL Snap cPL


• In dogs with more severe acute pancreatitis I think of it as AT BEST an • In the real world
“80%”test i.e. sensitivity and specificity is ~80%
• Acute abdomen
• 11 with pancreatitis
• 27 other (intestinal FB, hepatic or splenic masses, peritonitis)
• 4/5 dogs with acute pancreatitis will have a +ve spec cPL
Acute Abdomen SNAP cPL SNAP cPL
• 4/5 dogs that DO NOT have acute pancreatitis will have a –ve spec cPL +ve -ve

Pancreatitis 9/11 2/11


Other 11/27 16/27

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Snap cPL Spec cPL


• In the real world • In the real world
• Acute abdomen • Acute abdomen
• 11 with pancreatitis • 57 with pancreatitis
• 27 other (intestinal FB, hepatic or splenic masses, peritonitis) • 27 controls

Sensitivity Specificity Sensitivity Specificity

SNAP cPL 91-94% 71-78%


SNAP cPL 82% 59%

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SNAP cPL DGGR Lipase Assay


• Test is not very specific, so there will be a lot of false +ves • Results equivalent to pancreatic lipase in Ultrasound Dx of Ultrasound
dogs & cats Pancreatitis Normal
• Test is quite sensitive ~(80-)90% so won’t be too many false -ves DGGR Lipase 46/51
Pancreas
35/59
> 108 U/L
Spec cPL 41/51 32/59
• Because it is quite sensitive, if I get a –ve result this significantly lessens > 200 ug/L
DGGR Lipase 39/51 24/59
the chance my patient has pancreatitis . . . BUT it doesn’t rule it out > 216 U/L
Spec cPL 35/51 25/59
> 400 ug/L

J Vet Intern Med 2014;28:863–870

J Vet Intern Med 2013;27:1077–1082


J Am Vet Med Assoc 2014;244:1060–1065

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Other clinical pathology Peritoneal Fluid Analysis


The Veterinary Journal 201 (2014) 385–389
• Serum pancreatic elastase (PE-1)
• Results equivalent to pancreatic lipase • Not uncommon to see peritoneal fluid in severe acute pancreatitis
• Trypsinogen activation peptide (TAP) • 14 dogs with acute pancreatitis
• Not highly sensitive in dogs, not readily available • 19 with other conditions associated with abdominal fluid
• TLI
• Increases early in cases of experimental pancreatitis, followed by rapid • cPLI in the peritoneal fluid >500 ug/L
decrease
• Long turn around time • Sensitivity 100%
• Others have been assessed but not promising or readily available • Specificity 94.7%
• Phospholipase A2
• Trypsin-α1-anti-trypsin complexes

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Imaging - Radiology Imaging - Ultrasound


• Insensitive – Non-specific • What do you see?
• Of little use in diagnosis of pancreatitis • Irregularly enlarged, hypoechoic pancreatic tissue
• Hyperechoic peripancreatic fat
•  mass/cystic lesions
• MORE useful to rule out other differentials •  abdominal effusion
• Maybe
• thickening of adjacent gastric or intestinal walls Veterinary Ireland Journal
Volume 5 Number 5
• evidence of biliary obstruction
• intestinal ileus
• corrugation of the duodenum

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Aim of diagnostics
1. Find evidence to SUPPORT the diagnosis of pancreatitis

2. EXCLUDE alternative diagnoses, particularly SURGICAL INDICATIONS


• Obstruction
• Rupture History
• Torsion Physical examination
Imaging
• Perforation
Clinpath
• GDV
Exploratory surgery
• Biliary mucocoele
• Vascular occlusion

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Imaging - Ultrasound
• How good is it?
• sensitivity and specificity of ~70-80%

• Machine and operator dependent

• Ultrasound cannot distinguish:


• Pancreatitis from pancreatic neoplasia
• Acute from chronic pancreatitis

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Imaging - Ultrasound Imaging - CT


• Changes can mature with time – so don’t hesitate to have another • In people CT with IV contrast very sensitive (~90%) and specific
look (~90%)

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Imaging - CT Imaging - CT
J Vet Intern Med 2019;33:79–88
J Vet Intern Med 2015;29:97-103

• CT did no better than ultrasonography in 10 dogs

J Vet Intern Med 2019;33:79–88

• CT did no better than ultrasonography in 26 dogs

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Imaging - CT Imaging - CT
J Vet Intern Med 2019;33:79–88 J Vet Intern Med 2019;33:79–88
• 26 dogs with pancreatitis
• CT visualised the entire pancreas in 26/26 vs 19/26 with ultrasound
• Dogs with heterogenous contrast enhancement (indicates pancreatic
• CT and ultrasonography similar to detect signs of inflammation necrosis) had:
• CT slightly better pancreatic enlargement and gastric/intestinal thickening • Longer hospitalisation
• US slightly better peripancreatic fat/mesentery changes and detecting free • Higher cPL
fluid • More portal vein thrombosis
• Similar for extra-hepatic biliary obstruction
• CT did much better visualising portal vein thrombosis (10/26 vs 1/26)

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Imaging - MR Imaging - MR
• MRI detected
• Pancreatic abnormalities in 9/10 cats
• Scant data
• Peripancreatic abnormalities 1/10
• US detected
• Pancreatic abnormalities in 9/10 cats
• Peripancreatic abnormalities in 3/10
• Many of the changes were mild and only affected limited sections
and authors suggest the experience of the ultrasonographer was
very influential in detection

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Imaging - MR Pancreatic FNA


• 20-22g needle used
• “The advantages of MRI/MRCP over sonography of these cats included the • Non-aspiration (fenestration) or aspiration techniques
striking pancreatic signal changes associated with pancreatitis and the
ability to comprehensibly assess and measure the pancreas and
hepatobiliary structures without operator dependence or interference from
bowel gas. MRI/MRCP imaging of the feline abdomen may be beneficial in • Minimal and poor data on utility!!
cases with equivocal ultrasound imaging findings.”

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Journal of Feline Medicine and Journal of Feline Medicine and


Surgery 2015, 17(10) 858–863 Surgery 2015, 17(10) 858–863
Pancreatic FNA Pancreatic FNA

• 73 cats with pancreatitis and FNA vs 63 cats with FNA of another • Of the 73 cats with pancreatitis that had FNA
abdominal organ vs 61 cats with NO FNA • 24/73 non diagnostic
• No difference in rate of survival to discharge or length of hospital stay • ONLY 9 had histopathology for comparison and of these 6/9 there
between groups was agreement between cytology and histopathology (3 with
carcinoma, 3 with lymphocytic inflammation)
. . . So it is a safe procedure

93 94

Pancreatic FNA Pancreatic FNA


Journal of Veterinary Diagnostic
Investigation 2015 Vol 27: 236–240
• Retrospective study of 92 dogs that had undergone total of 94
pancreatic aspirates
• Diagnostic yield of 73.5% . . . • FNA cytology 26 dogs with acute pancreatitis
• 4/26 not attempted
• BUT histopathology only from 13 dogs (2 were inconclusive) • Concern for the safety of the procedure and patient care
• Cytology and histology agreed in 10/11 cases • 9/22 definitive evidence of inflammation (suppurative, pyogranulomatous,
mixed)
• 5 neoplasia & 5 inflammatory • 2/22 “possible” suppurative inflammation
• 1 dog cytology = inflammation and biopsy = normal • 11/22 inconclusive
• 7 adverse events recorded • Non-diagnostic samples
• No clinically relevant abnormalities
• 6 dogs had concurrent procedures performed and had co-morbidities • Mostly blood and fat
• 4 deaths

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Pancreatic FNA Pancreatic FNA


• 20-22g needle
• Potential problems include:
• Characteristics of inflammation overlap with malignancy
• FNA cytology 26 dogs with acute pancreatitis • Care with over-interpretation of malignancy!!
• 4/26 not attempted • Non representative sample obtained
• Concern for the safety of the procedure and patient care
• Hemodilution
• 9/22 definitive evidence of inflammation (suppurative, pyogranulomatous, • Other abdominal organ sampled
mixed)
• Uneven distribution of pathology in pancreas
• 2/22 “possible” suppurative inflammation
• Ruptured cells due to technique or innate fragility
• 11/22 inconclusive
• Necrotic tissue
• Non-diagnostic samples
• No clinically relevant abnormalities
• Mostly blood and fat 41% sensitivity

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Exploratory Laparotomy Exploratory Laparotomy


• MANY of the differentials for an acute abdomen are SURGICAL
PROS CONS
• Diagnostic if positive • Invasive
• “It is better to have a negative exploratory laparotomy than a
positive post mortem” • Placement of feeding tube • Costly
• Placement of biliary stent if • Not directly therapeutic – may
EHBDO exists worsen condition!
• Manage your client’s expectations
• Biopsy of other organs • Poor anaesthetic candidate?
• One pancreatic biopsy could
miss the diagnosis?

99 100

Aim of diagnostics Diagnosing Pancreatitis


1. Find evidence to SUPPORT the diagnosis of pancreatitis • There is NO single test – need to assess findings from multiple tests
2. EXCLUDE alternative diagnoses, particularly SURGICAL INDICATIONS • SNAP cPL useful (but not perfect) as a rule out test
• If –ve low chance patient has pancreatitis
• Ultrasound
• Helpful tool to diagnose pancreatitis
• Helpful tool to rule in or rule out other differentials
• Don’t hesitate to have another look in the following days
• All the other tests helpful but need careful interpretation
• Spec cPL, haemogram, serum biochemistry, FNA cytology

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Diagnosing Pancreatitis
• If you believe you have achieved a diagnosis of pancreatitis OR if you
have ruled out surgical differentials treatment will be similar and
supportive
• MONITOR your patient and QUESTION your diagnosis
• If patient stable or improving 
• Continue supportive care Treatment
• If patient deteriorating 
• Reassess diagnosis, repeat diagnostics

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Treatment – IV Fluids Treatment - Plasma


• Critical – patient will be dehydrated with • When to use? – no objective criteria
• Systemic effects • Does it help? – no objective criteria
• Local effect further compromising pancreatic microcirculation • Benefits
• Source of 1 protease inhibitor and 2 macroglobulins that bind circulating
• Theoretical benefit with lactated Ringer’s solution (Hartmanns) but trypsin and aid in the prevention of initiating the variety of detrimental
chemical cascades triggered by circulating proteolytic enzymes
may not translate to tangible benefit • Expand plasma volume (but only has ~30% oncotic effect cf colloids)
• Additional potassium supplementation
• Generally reserved for the more “severely” affected e.g.
• DIC is suspected
• Significant hypovolaemia consider colloids • Severely shocked patient

105 106

Treatment - Nutrition Treatment - Nutrition


• Starvation does not help any disease! • If anorexia persists beyond ~5 days then feeding tube will be required
• Gut contributes to systemic inflammation and depriving enterocytes • Naso-oesophageal / Oesophageal / Gastric / Jejunostomy
of luminal nutrients (especially amino acids) exacerbates problem
• Limited data that proves benefit of nutrition • No evidence on best food to provide
• Low fat seems sensible
• No evidence on correct amount of food
• If anorexia persists beyond ~5 days then feeding tube will be required • Something is better than nothing even if not achieving resting energy
• Naso-oesophageal / Oesophageal / Gastric / Jejunostomy requirement
• If patient vomiting reduce amount/frequency

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Treatment – Pain Relief Treatment - Antiemetics


• Commonly used examples: • Maropitant
• Buprenorphine • Metoclopramide
• 30-40 μg/kg q 4-6 hours • Ondansetron
• Taper by reducing dosage not frequency
• Ketamine CRI
• 20 μg/kg/min and taper slowly to effect (stop when reach 5 μg/kg/min)
• Lidocaine CRI
• 40 μg/kg/min and taper slowly to effect (stop when reach 10 μg/kg/min)
• Gabapentin
• 10 mg/kg PO q 12-24 hours
• Useful when discharge patient to home care

109 110

Treatment - Antibiotics Treatment – Gastric acid suppression


• Recent recognition of presence of bacteria in pancreatitis in cats and
dogs via translocation or via pancreatic duct • In theory:
• Can’t DDx sterile inflammation of acute pancreatitis vs inflammation • Decreased gastric acid production  decreased pancreatic secretion
associated with infection • Acute pancreatitis predisposes to gastric ulceration
• No general recommendation regarding antibiotic use • NO evidence to show benefit
• ?More severe cases with hypotension • Consider if signs suggest:
• ?Evidence of GIT compromise with melaena or haematochezia
• GI ulceration e.g. melaena, haematemesis
• ?Prolonged fasting
• Oesophagitis e.g. eructation, regurgitation, odynophagia
• ?Every case
• Amoxycillin – clavulanic acid suitable (broad coverage vs gut
pathogens)
• . . . BUT as always do not want to use antibiotics unnecessarily

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Treatment – Nasogastric suctioning Treatment – Managing Pancreatic Masses


• Many human studies show NO benefit • Terminology is REALLY confusing
• Some suggest exacerbate oesophagitis due to physical presence of
tube at gastro-oesophageal junction • Occur in up to ~7% of canine pancreatitis cases

• NOT recommended

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Treatment – Managing Pancreatic Masses Treatment – Managing Pancreatic Masses


• Pancreatic pseudocyst = collection of pancreatic juice enclosed within • Acute fluid collection in people = pancreatic fluid that develops within
wall of fibrous/granulation tissue 6 wks of acute pancreatitis
• Pancreatic necrosis = diffuse or focal area of nonviable pancreas +/- • Pancreatic pseudocyst in people = pancreatic fluid that develops >6
peripancreatic fat wks after acute pancreatitis
• Pancreatic abscess = collection of purulent material that may
associated with a +ve bacterial culture or sterile • Phlegmon = inspissated pancreatic tissue within 3 wks of acute
pancreatitis BUT this term also used to describe various lesions with
• Occur in up to ~7% of canine pancreatitis cases oedema, necrosis, infected or sterile purulent material, etc…

115 116

Treatment – Managing Pancreatic Masses Treatment - Corticosteroids


• Surgical management associated with high mortality rates – DON’T do • No data
it!!
• May exert many anti-inflammatory effects and trials underway in
• Ultrasound guided drainage – no proof of benefit BUT people
• If an abscess (particularly infected) then likely to be beneficial
• Relatively easy and minimal complications
• ?Role in critical illness associated corticosteroid insufficiency

• Might consider in severely affected patients with hypotension and


poor response to standard therapy

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Treatment - Corticosteroids JSAP 2019; 60: 298-304


Treatment - Corticosteroids
JSAP 2019; 60: 298-304

• 65 dogs with pancreatitis


• In addition to “standard” treatment (IVF, maropitant, fentanyl,
enrofloxacin, famotidine, multivitamin)
• 45 Rx prednisolone s/c 1 mg/kg/d until discharge
• 20 NO prednisolone
Number of days until CRP <2 mg/dL Number of days until clin score 2 or less Duration of hospitalisation

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Treatment - Corticosteroids Treatment - Corticosteroids JSAP 2019; 60: 298-304

JSAP 2019; 60: 298-304

• 1 mth survival
• Pred: 38/45 (88.7%)
• NO pred: 11/20 (57.9%)
• Study NOT blinded or randomised
• Relied on in-clinic test of lipase based on DGGR assay and did not
assay pancreatic specific lipase

121 122

Treatment – Pancreatic Enzyme Supplements Treatment


• Pancreatitis damages exocrine (and endocrine) pancreatic function • IV fluids
• Subclinical exocrine pancreatic insufficiency difficult to detect • Nutrition – anorexia 5+d
• ?Treat with enzyme supplements for 3-4 wks after discharge may be • Plasma – who and when??
of benefit • Pain relief
• Antiemetics
• Antibiotics?
• Gastric acid suppression?
• Corticosteroids?
• Pancreatic enzyme supplementation?

123 124

Follow up
• At discharge
• Low fat diet
• Avoid any known triggers (e.g. drug therapy)
• ?Pancreatic enzyme supplementation
• Check triglycerides +1-2 wks
• If ongoing hyperlipidaemia then investigate for causes and use low fat diet
• If not hyperlipidaemic then transition back to original diet

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