Contributors: James Simpson, Kenneth Simpson, Rance Sellon, Julien Bazelle

 Species: Canine   |   Classification: Diseases

Introduction Pathogenesis Diagnosis Treatment Outcomes Further Reading

Introduction

  • Edematous and necrotic/hemorrhagic forms.
  • Signs: acute abdominal pain, vomiting, depression and anorexia.
  • Diagnosis: biochemistry, hematology, ultrasonography.
  • Treatment: intravenous fluid support, antiemetics, analgesics, parenteral nutrition, plasma.
  • Prognosis: recurrence common.
    Print off the owner factsheet on Pancreatitis Pancreatitis to give to your client.Follow the management tree for vomiting/anorexia Vomiting in suspected pancreatitisDiagnostic tree: Vomiting.

Presenting Signs

  • Vomiting, diarrhea.
  • Cranial abdominal pain.
  • Anorexia.

Acute Presentation

  • Collapse.
  • Dyspnea.
  • Vomiting.

Age Predisposition

  • 4-8 years, variable.

Breed Predisposition

Cost Considerations

  • Intensive care in severe cases may be prolonged and expensive.

Pathogenesis

Etiology

  • Potential risk factors - cause usually unknown.
  • Unknown - predisposing factors:
    • Obesity.
    • High nutritional plane - high fat diets; high fat protein restricted diets.
    • Dietary indiscretion.
  • Hyperlipoproteinemia - primarily in:
  • Ischemia: hypotension, general anesthesia, compression of the pancreatic vessels during abdominal surgery.
  • Drugs, eg thiazides, furosemide, tetracyclines, azathioprine, high dose of corticosteroids (controversial and steroids may be indicated in some cases), particularly in patients with spinal trauma.
  • Infection - bacterial, viral, protozoal.
  • Duodenal reflux - not documented clinically.
  • Duct obstruction - edematous form, eg bile stones - rare.
  • Hypercalcemia Hypercalcemia: overview - particularly acute after IV calcium.
  • Trauma.
  • Uremia Uremia.
  • Auto-immune pancreatitis: suspected in English Cocker spaniel.
  • Idiopathic.

Predisposing Factors

General

  • Obesity/high plane of nutrition.
  • High dietary fat.
  • Diet indiscretion, eating table scraps.

Pathophysiology

  • Activation of zymogen granule enzymes within the pancreas, eg trypsinogen → trypsin.
  • Activation may be a consequence of hyperstimulation of pancreas → enzyme activation → pancreatic autodigestion.
  • Oxygen free radicals → damage to cell membranes → increased capillary permeability → edema.
  • Increased levels of cytokines, chemokines, proteases and phospholipase:
    • Locally increased permeability, thrombosis and necrosis.
    • Also have systemic effects.
  • Multisystem involvement includes disseminated intravascular coagulopathy (DIC), hypoalbuminemia Hypoproteinemia , vasculitis, pulmonary edema, acute renal failure Kidney: acute kidney injury (AKI) , cardiac arrhythmia Heart: dysrhythmia , liver damage.
  • Serum antiproteases help but rapidly used up, resulting in progression of enzymatic damage.

Timecourse

  • Acute progression - 24-48 h; consequently - may develop bile duct obstruction 5-10 d after acute bout or pseudocyst/abscess - variable time of onset 2-10 days? (DIC most common multi-system consequence).

Diagnosis

Presenting Problems

  • Vomiting.
  • Abdominal pain/acute abdomen.
  • Anorexia.
  • Fever.
  • Icterus.
  • Dyspnea.
  • Signs of colitis (mucus, fresh blood in stool; tenesmus) in some.

Client History

  • Vomiting.
  • Anorexia.
  • Icterus.
  • Dyspnea (pulmonary edema).
  • Diarrhea Diarrhea: overview that can have large bowel features.

Clinical Signs

  • Cranial abdominal pain.
  • Cardiac arrhythmia.
  • Icterus.
  • Abnormal lung sounds and tachypnea due to pulmonary edema.

Diagnostic Investigation

Biochemistry

Hematology

Radiography

  • Extremely poor sensitivity and specificity. Mainly performed to exclude other conditions and generally replaced by abdominal ultrasonography.
  • Lateral and dorsoventral abdominal Radiography: abdomen radiographs:
  • Poor contrast, especially in right upper quadrant of abdomen.
  • Left displacement of stomach, mass effect.
  • Increased angle between stomach and duodenum.
  • Gas in duodenum and/or ascending/transverse colon.

2-D Ultrasonography

  • Hypoechoic +/- enlarged pancreas with hyperechoic surrounding mesenteric fat Ultrasonography: pancreas Pancreas: normal - ultrasound.
  • Biliary obstruction (dilated cystic duct).
  • Fluid in abdomen: small quantity, often hyperechoic.
  • Corrugated small intestinal loops, decreased or increased intestinal motility.
  • Pancreatic cavitary lesion - pseudocyst/abscess. (uncommon complication).

Ascites: fluid analysis

  • Consistent with non septic exudate.
  • High cPLI or lipase values in the fluid have high sensitivity and specificity.

Histopathology Findings

  • Edematous changes, fat necrosis - localized and/or patchy.
  • Necrotizing, severe inflammatory changes and necrosis within pancreatic tissue and associated tissues.
  • Possibility of fibrosis in acute-on-chronic cases.

Differential Diagnosis

  • Vomiting Vomiting - many causes:
    • Primary gastrointestinal tract disease:
      • Dietary indiscretion/intolerance.
      • Intoxication.
      • Obstructive disease.
      • Inflammatory disease.
      • Ischemic disease.
      • Neoplasia (including paraneoplastic syndromes).
    • Secondary causes of vomiting:

Cranial abdominal pain

Icterus

Treatment

Initial Symptomatic Treatment

  • Intravenous fluid therapy (balanced electrolyte solution) Fluid therapy to promote pancreatic microcirculation, replace losses and for maintenance.
  • Antiemetics:
    • Maropitant Maropitant citrate (NK1 receptor antagonist; centrally acting).
    • Ondansetron Ondansetron or other 5HT 3 receptor antagonists.
    • Metoclopramide Metoclopramide : constant rate infusion may be more efficient than bolus. There is a theoretical risk of spasm of the Sphincter of Oddi with metoclopramide which is generally not observed clinically.
  • Pain relief: see discussion in standard treatment.
  • Nutritional support: early feeding is now considered the gold standard. This was found to improve outcome compared to parenteral nutrition, likely due to the decreased survival of enterocytes with glutamine deficiency. Recent studies showed good tolerance to early enteral feeding.
  • Feeding tube: naso-esophageal Nasoesophageal intubation , esophagostomy Esophagostomy or percutaneous endoscopically placed gastrostomy tubes Gastrostomy: percutaneous tube 1 (endoscopic) to allow feeding and to administrate medications (not possible with naso-esophageal feeding tubes).
  • Parenteral nutrition if vomiting >4-5 days, consider peripheral partial parenteral nutrition versus total parenteral nutrition.
  • Fresh frozen plasma to:
    • Restore anti-protease balance.
    • Treat DIC.
    • Restore albumin/globulin concentration.

Standard Treatment

  • Address any underlying causes if present.
  • Antimicrobials Therapeutics: antimicrobial drug , eg clavulanic acid Clavulanate -potentiated amoxicillin, amoxicillin Amoxicillin , metronidazole Metronidazole if pyrexic and leukocytosis evident, or confirmation of a septic process (eg fine needle aspiration of a cystic pancreatic lesion, consistent with pancreatic abscess).
    • Some clinicians feel that antimicrobials should only be used when there is evidence of an infectious complication or suspicion of a specific infectious disease.
  • Pethidine Pethidine is preferred to morphine for pain relief (fentanyl patch Fentanyl (transdermal patch) /buprenorphine).
    Do not use morphine as may stimulate closure of the Sphincter of Oddl, thus preventing pancreatic outflow.
  • Buprenorphine Buprenorphine may also cause spasm but effect is probably less marked than morphine.
  • Corticosteroid use controversial due to possible role in etiology and inhibition of clearance of circulating proteases by macrophages. If shocked, use as single intravenous bolus. In cases of auto-immune pancreatitis, these should be considered for long-term management (although it may be best not to use these during a severe acute episode).
  • Surgery - if severe or unresponsive or in the presence of pancreatic abscess, may perform laparotomy to lavage Laparotomy: midline :
    • Bile duct obstruction is not an absolute indication for surgery; biliary obstruction will resolve in most animal without surgical intervention.

Monitoring

  • Hydrations: adjust fluid rate and composition for maintenance and correct losses, eg vomiting.
  • Bleeding tendency: (monitor platelet count) may signal disseminated intravascular coagulopathy Disseminated intravascular coagulation.
  • Control pain.
  • Assess food intake.

Subsequent Management

Treatment

  • If progress poor, consider plasma transfusion** to supply serum antiproteases. Heparin and plasma for DIC. Recent study showed increased mortality rate in patients receiving regardless of the severity of the pancreatic disease and plasma transfusion should therefore be used with caution.
  • Surgery for unresponsive cases or cases of secondary extra-hepatic biliary tract obstruction.
  • Responsive cases:
    • Fat restricted diet <15% dry matter; avoid protein restricted high fat diets commonly used for struvite urolith dissolution.
    • Pancreatic enzyme replacer** 1 month or more if required. Pancreatic enzyme supplements may decrease the frequency and severity of acute episodes in human patients with chronic pancreatitis.
    • Control obesity.
    • Stop predisposing drugs if possible.

    **Not proven in clinical trials to improve outcomes in dogs with acute pancreatitis, but of potential benefit with little risk of side effects.

Monitoring

  • Repeat physical examinations, ultrasound, and routine CBC/biochemistry.
    • Repeat PLI, TLI (mainly to assess development of EPI, not useful for diagnosis and monitoring of pancreatic inflammation), amylase and lipase assay to monitor leakage of pancreatic enzymes:
      • Clinical judgement should rule; some dogs that have returned to clinical normalcy and are ready for oral alimentation may retain high serum amylase or lipase activity for a period of time.
      • Normalized PLI does not completely exclude the progression to chronic pancreatitis.

Outcomes

Prognosis

  • Fair prognosis in short-term unless necrotizing, then prognosis is very poor.
  • Recurrence common.
  • Possibility to progress to chronic pancreatitis.
  • Negative prognostic factors: dyslipidemia.

Expected Response to Treatment

  • No vomiting within 24 h.
  • Appetite returns and improvement in general demeanor in 3-4 days.
  • Able to cope with normal diet within 4-5 days.

Reasons for Treatment Failure

  • Severe necrotizing pancreatitis.
  • Development of disseminated intravascular coagulation, sepsis or other systemic complications.
  • Development of bile duct obstruction.
  • Development of pancreatic phlegm (solid benign mass) → pancreatic pseudocyst → sterile necrosis and pancreatic abscess → poor prognosis.
  • Rule out pancreatic cancer Pancreas: neoplasia where recurrent/unresponsive.

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Harris J P, Parnell N K, Griffith E H, Saker K E (2017) Retrospective evaluation of the impact of early enteral nutrition on clinical outcomes in dogs with pancreatitis: 34 cases (2010-2013). J Vet Emerg Crit Care (San Antonio) 27(4), 425-433 PubMed.
  • Pratschke K M, Ryan J, McAlinden A & McLauchlan G (2015) Pancreatic surgical biopsy in 24 dogs and 19 cats: postoperative complications and clinical relevance of histological findings. J Small Anim Pract 56 (1), 60-66 PubMed.
  • Chartier M A, Hill S L, Sunico S, Suchodolski J S, Robertson J E & Steiner J M (2014) Pancreas-specific lipase concentrations and amylase and lipase activities in the peritoneal fluid of dogs with suspected pancreatitis. Vet J 201 (3), 385-389 PubMed.
  • Haworth M D, Hosgood G, Swindells K L & Mansfield C S (2014) Diagnostic accuracy of the SNAP and Spec canine pancreatic lipase tests for pancreatitis in dogs presenting with clinical signs of acute abdominal disease. J Vet Emerg Crit Care (San Antonio) 24 (2), 135-143 PubMed.
  • Paek J, Kang J H, Kim H S, Lee I, Seo K W & Yang M P (2014) Serum adipokine concentrations in dogs with acute pancreatitis. J Vet Intern Med 28 (6), 1760-1769 PubMed.
  • McCord K, Morley P S, Armstrong J, Simpson K, Rishniw M, Forman M A, Biller D, Parnell N, Arnell K, Hill S, Avgeris S, Gittelman H, Moore M, Hitt M, Oswald G, Marks S, Burney D & Twedt D (2012) A multi-institutional study evaluating the diagnostic utility of the spec cPL" and SNAP® cPL" in clinical acute pancreatitis in 84 dogs. J Vet Intern Med 26 (4), 888-896 PubMed.
  • Mansfield C (2012) Pathophysiology of acute pancreatitis: potential application from experimental models and human medicine to dogs. J Vet Intern Med 26 (4), 875-87 PubMed.
  • Trivedi S, Marks S L, Kass P H, Luff J A, Keller S M, Johnson E G & Murphy B (2011) Sensitivity and specificity of canine pancreas-specific lipase (cPL) and other markers of pancreatitis in 70 dogs with and without histopathologic evidence of pancreatitis. J Vet Intern Med 25 (6), 1241-1247 PubMed.
  • Mansfield C S, James F E, Steiner J M, Suchodolski J S, Robertson I D & Hosgood G (2011) A pilot study to assess tolerability of early enteral nutrition via esophagostomy tube feeding in dogs with severe acute pancreatitis. J Vet Intern Med 25 (3), 419-425 PubMed.
  • Weatherton L K & Streeter E M (2009) Evaluation of fresh frozen plasma administration in dogs with pancreatitis: 77 cases (1995-2005). J Vet Emerg Crit Care (San Antonio) 19 (6), 617-622 PubMed.
  • Lem K Y, Fosgate G T, Norby B & Steriner J M (2008) Associations between dietary factors and pancreatitis in dogs. J Am Vet Med Assoc 233 (9), 1425-1431 PubMed.
  • Mansfield C S, James F E, Robertson I D (2008) Development of a clinical severity index for dogs with acute pancreatitis. JAVMA 233 (6), 936-944 PubMed.
  • Flint RS & Windsor JA (2003) The role of the intestine in the pathophysiology and management of severe acute pancreatitis. HPB (Oxford) 5 (2), 69-85 PubMed.
  • Holm J L, Chan D L & Rozanski E A (2003) Acute pancreatitis in dogs. J Vet Emerg Crit Care 13 (4), 201-213 VetMedResource.
  • Steiner J M, Broussard J, Mansfield C S, Gumminger S R & Williams D A (2001) Serum canine pancreatic lipase immunoreactivity (cPLI) concentrations in dogs with spontaneous pancreatitis. JVIM 15, 274 Research Gate.
  • Mansfield C S & Jones B R (2000) Plasma and urinary trypsinogen activation peptide in healthy dogs, dogs with pancreatitis and dogs with other systemic diseases. Aust Vet J 78 (6), 416-422 PubMed.
  • Hess R et al (1998) Clinical, clinicopathologic, radiographic and ultrasonographic abnormalities in dogs with fatal acute pancreatitis: 70 cases. JAVMA 213 (5), 665-670 PubMed.
  • Ruaux C & Atwell R B (1998) A severity score for spontaneous canine acute pancreatitis. Aust Vet J 76 (12), 804-8 PubMed.
  • Williams D (1994) Diagnosis and management of acute pancreatitis. JSAP 35 (9), 445-454 VetMedResource.
  • Simpson et al (1989) Circulating concentrations of TLI and activities of serum amylase and lipase after pancreatic duct ligation in dogs. Am J Vet Res 50 (5), 629-632 PubMed.

Other sources of information

  • Mansfield C (2004)New directions in diagnosing and treating canine pancreatitis.Proceedings of the ACVIM Forum 2004, Minneapolis, June 9-12, 2004.
  • Williams D & Steiner J (2000)Canine pancreatitis.In:Current Veterinary Therapy XIII.J Bonagura (ed), W B Saunders. pp 687-701.

Other Sources of Information