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Pancreatitis (veterinary)

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Illustration of a dog's pancreas: Alveolus in the illustration refers to the acinar cells of the exocrine pancreas. The cells form circular clusters.[1] They are the cells which produce pancreatic enzymes needed for digestion of food.

Pancreatitis is a common condition in cats and dogs. Pancreatitis is inflammation of the pancreas that can occur in two very different forms. Acute pancreatitis[2] is sudden, while chronic pancreatitis is characterized by recurring or persistent form of pancreatic inflammation. Cases of both can be considered mild or severe.[3] It is currently undecided whether chronic pancreatitis is a distinct disease or a form of acute pancreatitis. Other forms such as auto-immune and hereditary pancreatitis are presumed to occur but there existence has not been proven.[4]

Pancreatitis occurs in approximately 0.8% of dogs and 0.6% of cats. Severe pancreatitis is often fatal.[4]

Background

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The pancreas is composed of two sections: the smaller endocrine portion, which is responsible for producing hormones such as insulin, somatostatin, and glucagon, and the larger, exocrine portion,[5] which produces enzymes needed for the digestion of food. Acinar cells make up 82% of the total pancreas; these cells are responsible for the production of the digestive enzymes.[1][6]

Pathogenesis

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The pathogenesis of pancreatitis is not well understood. Both genetic and environmental factors are involved in developing pancreatitis. In most acute pancreatitis cases there is premature activation and retention of zymogens of the acinar cells. These zymogens become pancreatic enzymes. Activated enzymes will get into the pancreatic tissue and later the peritoneal cavity and circulation. The effects of this include: interstitial oedema, necrosis of the acinar cells, haemorrhage, and necrosis of the peripancreatic fat; these trigger an inflammatory response from neutrophils and macrophages. The aetiology behind this disruption is unknown.[4]

Pathophysiology

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Pancreatitis is caused by autodigestion of the pancreas thought to begin with an increase in secretion of pancreatic enzymes in response to a stimulus,[7][8] which can be any source from table scraps to getting into the garbage to drugs, toxins, and trauma.[3][9] The digestive enzymes are released too quickly and begin acting on the pancreas instead of the food they normally digest.[2][9][10][11] Once the process cascades, inflammatory mediators and free radicals are released and pancreatitis develops, causing amplification of the process.[10]

Causes

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The aetiology of pancreatitis in cats and dogs is unknown in the majority of cases. The amount of described causes for dogs is low and even lesser for cats. The causes of pancreatitis in humans is vastly different from that of cats and dogs.[4] Two studies have suggested that hypertriglyceridaemia is a cause of pancreatitis in the Miniature Schnauzer;[12][13] however, there is no evidence of this as a cause in other breeds.[4] Another study has identified mutations of the SPINK1 gene in the Miniature Schnauzer as being associated with pancreatitis;[14] however, another study found no association between SPINK1 mutations and pancreatitis instead demonstrated that the mutations were common amongst Schnauzers.[15][4]

Iatrogenic pancreatitis is caused by certain drugs. The most common drugs that cause iatrogenic pancreatitis are potassium bromide, phenobarbital, L-asparaginase, azathioprine, and meglumine antimonate.[4]

Suspected causes of pancreatitis in cats includes: abdominal trauma, ischaemia, acute hypercalcaemia, organophosphate toxicity, pancreatic tumour, and pancreatic ductal obstruction.[4]

Clinical signs

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Clinical symptoms of pancreatitis vary. Some animals will be asymptomatic or just have mild anorexia whilst others will have serious symptoms such as cardiac problems. Most symptoms are not directly caused by pancreatitis itself.[4]

One study found the most common symptoms of pancreatitis in dogs to be: lethargy (88%), anorexia (86%), emesis (83%), and abdominal pain (59%).[16][4]

Symptoms common in cats with pancreatitis include: anorexia (63–97%), dehydration (33–96%), lethargy (28–100%), emesis (35–76%), pallor (30%), icterus (16–24%), weight loss (20–61%), and diarrhoea (11–33%).[4]

Symptoms of severe pancreatitis in cats includes: disseminated intravascular coagulation, pulmonary thromboembolism, cardiovascular shock, and organ failure. Pancreatitis is a common cause of disseminated intravascular coagulation and thromboembolism in the cat. Two studies found 26% of cats with disseminated intravascular coagulation and 11.8% with pulmonary thromboembolism had pancreatitis.[4]

Acute pancreatitis can trigger a build-up of fluid, particularly in abdominal and thoracic (chest) areas, acute kidney injury, and cause inflammation in arteries and veins. The inflammation triggers the body's clotting factors, possibly depleting them to the point of spontaneous bleeding.[9][17] This form can be fatal in animals and in humans.[18] Severe acute pancreatitis also causes cardiovascular shock, disseminated intravascular coagulation, systemic inflammatory response syndrome, and organ failure.[4] Dehydration is observed in nearly all dogs with severe acute pancreatitis.[4]

Serious and severe symptoms that are not uncommon include: hypokalaemia, hyponatraemia, and hypochloraemia. Hyperkalaemia, hypernatraemia, and hypocalceamia are reported but rare.[4]

Pancreatitis can result in exocrine pancreatic insufficiency, if the organ's acinar cells are permanently damaged; the pancreatic enzymes then need replacement with pancrelipase or similar products. The damage can also extend into the endocrine portion of the pancreas, resulting in diabetes mellitus.[19] Whether the diabetes is transient or permanent depends on the severity of the damage to the endocrine pancreas beta cells.[17]

Risk factors

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Although various causes of dog pancreatitis are known, such as drugs, fatty diet, trauma, etc., the pathophysiology is very complex.[2][20] Pancreatitis can be idiopathic; no real causation factor can be found.[10][18] Obese animals as well as animals fed a diet high in fat may be more prone to developing acute and chronic pancreatitis.[2][21][22] Certain breeds of dogs are considered predisposed to developing pancreatitis including Miniature Schnauzers, Cocker Spaniels, and some terrier breeds.[9][10][21][23] Miniature Schnauzers as a breed tend toward developing hyperlipidemia, an excess of circulating fats in the blood.[24] The breed that appears to be at risk for the acute form of pancreatitis is the Yorkshire Terrier, while Labrador Retrievers and Miniature Poodles seem to have a decreased risk for the acute form of the disease. Genetics may play a part in the risk factor.[2] Certain cat breeds may have a predisposition.[4] Dogs suffering from diabetes mellitus, Cushing's disease (hyperadrenocorticism), hypothyroidism, and epilepsy have been reported to have an increased risk but no there is a lack of evidence to support a link between the conditions and pancreatitis.[4] Diabetes and hypothyroidism are also associated with hyperlipidemia.[25][26] Those with other types of gastrointestinal conditions and dogs that have had previous pancreatitis attacks are also at increased risk for the disorder.[2]

In cats, a study found an association with inflammatory bowel disease and cholangitis with pancreatitis.[27] Triaditis is a medical condition/term for when a cat has all three conditions. 50–67% of cats with pancreatitis have triaditis. In cats with cholangitis 50–80% have pancreatitis. The cause of this and the relationship between the conditions is not understood.[4]

There is no sex predilection.[4]

Age of onset

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Pancreatitis can occur at any age but most animals with pancreatitis are middle-aged to elderly.[4]

Diagnosis

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Histopathological methods of diagnosis have been reported to diagnose up to 90% of clinically healthy dogs and 65% of cats with pancreatitis. Histopathology is not recommended for the diagnosis of pancreatitis on its own.[4]

Complete blood count, serum biochemistry, and urinalysis are not helpful for diagnosing pancreatitis; however, they are useful to exclude differential diagnosis and confirm comorbidities.[4]

Haemotological findings that can occur include: anaemia, leukopaenia, and thrombocytopaenia. These are not indicative of pancreatitis but instead symptoms of it.[4]

Pancreatic lipase assay

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Pancreatic lipase is an enzyme produced by the acinar cells of the pancreas. This makes measurement of it the most effective way to diagnose pancreatitis. Pancreatic lipase immunoreactivity assays are the most accurate type of assay for this. The sensitivity for these assays are quite accurate.[4]

Serum amylase and lipase activities

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Serum amylase and lipase activities are not a useful indicator for pancreatitis as it can be synthesised by non-pancreatic tissue and the tests cannot distinguish the tissue origin. In one study 50% of dogs with increased amylase and lipase activities did not have any other evidence of pancreatitis. In cats the test has little to no clinical use.[4]

Trypsin-like immunoreactivity

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Serum trypsin-like immunoreactivity assays measure the amount of trypsinogen and trypsin in the serum. The tests are different for cats and dogs. In dogs results indicative of pancreatitis may also be caused by renal failure and enteropathies. In cats low sensitivity and other conditions—gastrointestinal diseases, azotemia—that produce similar results mean it is not a useful tool for diagnosis of pancreatitis.[4]

Radiography

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The majority of cats and dogs with pancreatitis show no abnormalities on radiographs. Instead radiography serves as a way to diagnose or exclude other conditions. Findings possible in animals with pancreatitis include:f increased opacity of soft tissue, a decrease in serosal detail in the cranial right abdomen, gastric displacement, duodenum displacement, ascites, and a cranial abdominal mass.[4]

Ultrasound

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Ultrasonography of the abdomen is the best method of diagnosing pancreatitis in cats and dogs. Due to advances in ultrasonography it is a routine procedure for diagnosing pancreatitis. Hypoechoic areas within the pancreas, an increase in echogenicity of the mesentery around the pancreas, and pancreatic abnormalities are all common ultrasonographic findings in cases of pancreatitis. Some patients with pancreatitis will not present with any ultrasonographic abnormalities.[4]

Pathology

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Tissue samples should be collected from pancreatic lesions that can be seen during surgery. These lesions may include peripancreatic fat necrosis, pancreatic haemorrhage, and pancreatic congestion. Lesions are not always present and cannot always be distinguished from nodular hyperplasia and neoplasia.[4]

Histopathology can differentiate acute and chronic pancreatitis. Pancreatic fibrosis and acinar atrophy suggest chronic instead of acute pancreatitis.[4]

Cytology

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Cytological examination of the pancreas can be done with fine needle aspiration. This is less invasive than histopathology. FNA can differentiate acute pancreatitis, on a smear there will be hypercellularity and degraded neutrophils.[4]

Treatment

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Due to the unknown aetiology treatment is supportive and based on what symptoms the animal shows. Underlying conditions such as infections, toxicity, and endocrinopathies, etc. should be treated.[4]

Fluid therapy

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Severe pancreatitis can cause dehydration and hypovolaemia, this can be treated with intravenous fluid therapy. When the patient has hypoalbuminaemia or hypotension colloid fluids should be used instead of crystalloid fluids that are normally used.[4]

Feeding

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Historically it was believed withholding food was beneficial, this is no longer the case. Current practice is to provide enteral and parenteral alimentation. Jejunal feeding is the preferred method for this.[4]

Postpancreatitis management

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A low-fat diet is indicated.[3] The use of drugs that are known to have an association with pancreatitis should be avoided.[20][17] Some patients benefit from the use of pancreatic enzymes on a supplemental basis. One study indicated that 57% dogs followed for six months after an acute pancreatitis attack, either continued to exhibit inflammation of the organ or had decreased acinar cell function, though they had no pancreatitis symptoms.[20][28]

See also

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References

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  1. ^ a b "Gross and Microscopic Anatomy of the Pancreas". Colorado State University School of Veterinary Medicine. Archived from the original on 14 May 2011. Retrieved 8 April 2011.
  2. ^ a b c d e f Washabau, Robert J. (2009). "Canine Pancreatic Disease: What's New in Diagnosis and Therapy?". 34th Congress-World Small Animal Veterinary Association (WSAVA). Retrieved 8 April 2011.
  3. ^ a b c Steiner, Jörg M. (August 2003). "Pancreatitis" (PDF). Clinician's Brief-North American Veterinary Conference. Retrieved 9 April 2011.
  4. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah Monnet, Eric; Steiner, Jorg M.; Xenoulis, Panagiotis G. (12 May 2023). "Pancreatitis". Small Animal Soft Tissue Surgery. Wiley. pp. 230–250. doi:10.1002/9781119693741. ISBN 978-1-119-69368-0.
  5. ^ "Exocrine Sections of the Pancreas". Colorado State University School of Veterinary Medicine. Archived from the original on 14 May 2011. Retrieved 8 April 2011.
  6. ^ "Acinar Cell". Auckland Bioengineering Institute-University of Auckland. Archived from the original on 26 February 2008. Retrieved 8 April 2011.
  7. ^ "Enteric Endocrine System". Colorado State University School of Veterinary Medicine. Archived from the original on 14 May 2011. Retrieved 8 April 2011.
  8. ^ "Control of Pancreatic Exocrine Secretion". Colorado State University School of Veterinary Medicine. Archived from the original on 14 May 2011. Retrieved 8 April 2011.
  9. ^ a b c d "Big Steak Dinner" (PDF). Tufts School of Veterinary Medicine. 2007. Retrieved 8 April 2011.
  10. ^ a b c d West, Laura D.; Almy, Frederic S. "Diagnosing Pancreatitis in Dogs and Cats by Laboratory Methods". University of Georgia School of Veterinary Medicine. Retrieved 8 April 2011.
  11. ^ J. M. Steiner (2003). "Diagnosis of acute pancreatitis". Vet Clin North Am Small Anim Pract. 33: 1181–1195.
  12. ^ Xenoulis, Panagiotis G.; Suchodolski, Jan S.; Ruaux, Craig G.; Steiner, Jörg M. (1 July 2010). "Association Between Serum Triglyceride and Canine Pancreatic Lipase Immunoreactivity Concentrations in Miniature Schnauzers". Journal of the American Animal Hospital Association. 46 (4). American Animal Hospital Association: 229–234. doi:10.5326/0460229. ISSN 0587-2871.
  13. ^ Xenoulis, P.G.; Levinski, M.D.; Suchodolski, J.S.; Steiner, J.M. (8 December 2010). "Serum Triglyceride Concentrations in Miniature Schnauzers with and without a History of Probable Pancreatitis". Journal of Veterinary Internal Medicine. 25 (1). Wiley: 20–25. doi:10.1111/j.1939-1676.2010.0644.x. ISSN 0891-6640.
  14. ^ Bishop, Micah A.; Xenoulis, Panagiotis G.; Levinski, Melinda D.; Suchodolski, Jan S.; Steiner, Jörg M. (2010). "Identification of variants of the SPINK1 gene and their association with pancreatitis in Miniature Schnauzers". American Journal of Veterinary Research. 71 (5). American Veterinary Medical Association (AVMA): 527–533. doi:10.2460/ajvr.71.5.527. ISSN 0002-9645.
  15. ^ Furrow, E.; Armstrong, P.J.; Patterson, E.E. (13 October 2012). "High Prevalence of the c.74A>C<scp>SPINK</scp>1Variant in Miniature and Standard Schnauzers". Journal of Veterinary Internal Medicine. 26 (6). Wiley: 1295–1299. doi:10.1111/j.1939-1676.2012.01013.x. ISSN 0891-6640.
  16. ^ Berman, Chad F.; Lindquist, Eric; Lobetti, Remo G. (2020). "Comparison of clinical findings in 293 dogs with suspect acute pancreatitis : different clinical presentation with left lobe, right lobe or diffuse involvement of the pancreas". Journal of the South African Veterinary Association. 91 (1). Medpharm Publications: 1–10. doi:10.4102/jsava.v91i0.2022. ISSN 1019-9128. PMC 7203193.
  17. ^ a b c Brooks, Wendy C. "Canine Pancreatitis". Veterinary Partner. Retrieved 8 April 2011.
  18. ^ a b "Pancreatitis". Merck Veterinary Manual. Retrieved 8 April 2011.
  19. ^ Hoskins, Johnny D. (2002). "Can You Rule Out Pancreatitis?". DVM 360. Retrieved 8 April 2011.
  20. ^ a b c "Diagnosing and Treating Pancreatitis" (PDF). IDEXX Laboratories. 2006. p. 3. Archived (PDF) from the original on 4 March 2016. Retrieved 21 April 2011.
  21. ^ a b Armstrong, P. Jane (2011). "Canine Pancreatitis: Diagnosis and Management" (PDF). Western Veterinary Conference. Archived from the original (PDF) on 29 March 2016. Retrieved 8 April 2011.
  22. ^ Williams DA, Steiner JM. Canine Exocrine Pancreatic Disease. In Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine, Diseases of the Dog and Cat, 6th ed. St. Louis, Elsevier Saunders, 2005, pp. 1482-1487
  23. ^ Simpson, KW. Diseases of the Pancreas. In Tams T. (ed): Handbook of Small Animal Gastroenterology, 2nd ed. St. Louis, W. B. Saunders Co, 2003, pp. 353-365.
  24. ^ Xenoulis, Panagiotis G.; Suchodolski, Jan S.; Levinski, Melinda D.; Steiner, Jörg M. (2007). "Investigation of Hypertriglyceridemia in Healthy Miniature Schnauzers". Journal of Veterinary Internal Medicine. doi:10.1111/j.1939-1676.2007.tb01942.x.
  25. ^ Herrtage, Michael (2009). "New Strategies in the Management of Canine Diabetes Mellitus". WSAVA. Retrieved 8 April 2011.
  26. ^ "Abstract #216-Association Between Hyperlipidemia & Hypothyroid in Dogs" (PDF). American College of Veterinary Internal Medicine. 2004. p. 81. Retrieved 8 April 2011.
  27. ^ DJ, Weiss; JM, Gagne; PJ, Armstrong. "Relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis, and nephritis in cats". Journal of the American Veterinary Medical Association. 209 (6). J Am Vet Med Assoc. ISSN 0003-1488. PMID 8800259. Retrieved 14 August 2024.
  28. ^ "Mild Chronic Pancreatitis". Merck Veterinary Manual. Retrieved 8 April 2011.