Pancreatitis

Jump to... Pathogenesis Diagnosis Treatment Prevention Sequelae Sources

• Signs: often vague (lethargy, anorexia); or asymptomatic.
• Diagnosis: elevated trypsin-like immunoreactivity (TLI), ultrasonography, histopathology.
• Treatment: intravenous fluid support, dietary modification, enteral/parenteral nutrition.
• Prognosis: guarded.

• May be no clinical signs.

• Recognized in association with cholangiohepatitis , triaditis, and/or inflammatory bowel disease or hepatic lipidosis and signs may be indistinguishable from these:
  • Anorexia/weight loss.
  • Vomiting.
  • Cranial abdominal pain.

• Peracute with signs of shock, pleural/peritoneal effusions have been reported but are rare.

• Most commonly reported in North America but increasingly recognized in European cats.

• Young to middle aged adult (mean age ~5 years).

• +/- higher incidence in Siamese .

• Idiopathic (most common).
• Other possibilities include:
  • Biliary tract inflammation (may be associated with cholangiohepatitis but pancreatitis tends to be mild in these cases).
  • Inflammatory bowel disease .
  • Metabolic, eg hypercalcemia  and hyperlipidemia .
  • Infection: feline leukemia virus , Toxoplasma gondii , feline herpes virus .
  • Aberrant migration of liver flukes .
  • Drugs, eg organophosphates .
  • Pancreatic ischemia/trauma, eg RTA, surgery.
  • Vomiting can raise intraduodenal pressure and predispose to reflux of enteric contents into the pancreatic duct.

• Hyperstimulation of pancreas.
• Blocked pancreatic ducts.

• Hyperstimulation of pancreas or blocked pancreatic duct fusion of zymogen granules and lysozymes activation of intrapancreatic trypsin and pancreatic autodigestion.
• Oxygen-derived free radicals damage to cell membranes increased capillary permeability edema.
• Increased levels of proteases and phospholipase in pancreas and blood stream necrosis multisystem involvement including pulmonary edema. Trypsin activates coagulation cascade and fibrinolytic system can disseminated intravascular coagulation.
• Serum antiproteases and alpha-2 macroglobulin bind trypsin and are removed from circulation. Manifestations of pancreatitis are only seen when compensatory mechanisms are overwhelmed.

• Acute progression: 24-48 hours, but many cats appear to have chronic relapsing pancreatitis.

• Anorexia.
• Weight loss.
• Vomiting .
• Icterus.

• May be no clinical signs.
• Anorexia.

• Lethargy.
• Dyspnea.
• Diarrhea.
• Vomiting (35% cases).

• Ataxia.

• Some cases subclinical.
• Dehydration.
• Thin/poorly muscled.

• Cranial abdominal pain in 25% cases (more often associated with experimental disease).
• Hypothermia (although some cases may be pyrexic).
• Palpable abdominal mass.

• Hepatomegaly.
• Icterus.

• Occasionally dyspnea.

• Is supportive of pancreatic abnormalities.
• Free peritoneal fluid is often visible .
• Pancreas is often very difficult to image but may be seen as hypoechoic or heterogenous mass.
• May detect concomitant liver and GI disease.
• Recently endosonography has been trialled for diagnosis but was not shown to be any better than ultrasonography except perhaps in obese cats where standard ultrasounds are difficult.

• Feline trypsin-like immunoreactivity (FTLI) .
• Serum pancreatic lipase immunoreactivity (fPLI) - recently developed and validated. Test is specific for pancreatitis.
• Often mild or non-specific even in severe cases.
• Azotemia ; usually prerenal.
• Elevated hepatic enzymes are a common finding (may be due to secondary hepatic lipidosis ).
• Hypokalemia and hypophosphatemia .
• Hyperglycemia or hypoglycemia .
• Hyperlipidemia .
• Hypocalcemia .
• Hypoalbuminemia may occur which results in hypocalcemia on blood sample.
• Hyperbilirubinemia .
   Lipase and amylase concentrations usually within normal range.

Hematology

• Thrombocytopenia may contribute to coagulopathy.
• Anemia (non-regenerative>regenerative) may be present, or in 13% cases increased PCV due to dehydration.
• Neutrophilia often not marked, and 15% cases show leukopenia.
• Coagulation abnormalities are very common, prothrombin time and thromboplastin time are frequently prolonged.
• Vitamin K deficiency is common in cats with pancreatitis, inflammatory bowel disease or liver disease.

• Rarely specific or diagnostic.
• Poor abdominal contrast due to localized peritonitis or fluid accumulation on lateral and dorsoventral abdominal radiographs.
• Hepatomegaly is a common finding .

Computed tomography

• The normal pancreas is readily idenitfied using CT - it is homogenous with smooth margins.
• The value of CT in identifying pancreatitis is under debate.

• Clinical signs.

• Elevated TLI: TLI often elevated in cats with inflammatory bowel disease.
• Ultrasonography: normal pancreas does not rule it out.
• Exploratory laparotomy and pancreatic biopsy is often warranted to achieve definitive diagnosis and to biopsy GIT and liver.

• Check for other concurrent disease, eg enteropathy, liver disease.
• Do not confuse nodular pancreatic hyperplasia (common incidental finding) with lesion.
• Examine promptly and handle pancreatic tissue gently.

• Variable infiltration of pancreatic tissues with neutrophils/lymphocytes.
• Mild to severe pancreatic necrosis and hemorrhage.
• +/- peripancreatic fat necrosis.

• Variable degree of fibrosis depending on chronicity.

• Cholangiohepatitis and IBD are commonly seen in association with pancreatitis.
• Pulmonary thrombi.

• Inflammatory bowel disease (may be concurrent disease).
• Intestinal foreign body .
• Cholangiohepatitis (may be concurrent disease).
• Feline infectious peritonitis .

• Panleukopenia .
• Peritonitis .

• Steatitis.
• Neoplasia .
• Causes of icterus:
  • Hepatitis .
  • Cholangiohepatitis .
  • Intravascular hemolysis .

• Hepatic lipidosis .

• Remove inciting cause if possible.

• Intravenous fluid therapy to replace losses and for maintenance. Plasma 10-20 mg/kg if reduced protein or non-responsive to electrolyte therapy.
• No evidence that starvation improves prognosis in cats as most have been anorectic >1 week prior to diagnosis but if the cat is vomiting a regime of nil per os should be adopted for 2-3 days (in other cases can feed through disease).
• Anti-emetics are seldom required.
• Re-introduce or feed a diet with low fat, high carbohydrate composition.
• In cats with pancreatitis or hepatic lipidosis, oral nutrition is often inadequate and aggressive enteral nutrition via gastrostomy tubes or enterostomy tubes has been recommended. Parenteral nutrition if enteral nutrition is not tolerated.
• Control DIC - plasma/heparin.

• The use of antiobiotics is controversial.
• Amoxicillin may be used but no proven beneficial effect.
• The importance of analgesia is easily overlooked as evidence of abdominal pain is not easy to detect in cats.
  • Acute pain control
    • Hydromorphone IM .
    • Buprenorphine IM or via buccal mucous membranes .
    • Intraperitoneal low-dose bupivicaine .
  • Longer duration pain control
    • Fentanyl patch .
    • Epidural analgesia.

• Treat other conditions such as inflammatory bowel disease or liver disease.

• Butorphanol 0.1-0.4 mg/kg SC QID for pain relief or oxymorphone 0.05-0.1 mg/kg SC q6h.
   Do not use morphine as this may stimulate closure of the sphincter of Odi, thus preventing pancreatic flow.

• Hydration: adjust fluid rate for maintenance.
• Bleeding tendency: may signal disseminated intravascular coagulopathy.
• Test for and treat vitamin K deficiency.
• Blood [glucose] for monitoring transient or permanent diabetes mellitus.

• If progress poor, consider blood or plasma transfusion to supply serum antiproteases.
• Feed low fat, high carbohydrate diet.

• Prognosis very variable - related to extent of pancreatic necrosis and presence of complications.
• Very poor prognosis for suppurative pancreatitis.
• Poor prognosis if associated with concurrent disease (survival rate probably <50%).

• Appetite returns and improvement in general demeanor in 3-4 days.

• Severe necrotizing pancreatitis overwhelming compensatory mechanisms.
• Development of disseminated intravascular coagulation.
• Development of pancreatic pseudocyst sterile necrosis and pancreatic abscess poor prognosis.
• Development of renal failure.

• Recent references from PubMed.
• Steiner J M (2003) Diagnosis of pancreatitis. Vet Clin North Am Small Anim Pract. 33 (5), 1181-1195. PubMed (Contains information about serum fPLI test)
• Simpson K W (2002) Feline pancreatitis. J Feline Med Surg. 4 (3), 183-184. PubMed
• Mansfield C S & Jones B R (2001) Review of feline pancreatitis part 1 - the normal feline pancreas, the pathophysiology, classification, prevalence and aetiologies of pancreatitis. JFMS 3, 117-124. PubMed
• Mansfield C S & Jones B R (2001) Review of feline pancreatitis part 2 - clinical signs, diagnosis and treatment. JFMS 3, 125-132. PubMed
• Washabau R J (2001) Feline acute pancreatitis - important species differences. JFMS 3, 95-98. PubMed
• Gerhardt A, Steiner J M, Williams D A, Kramer S, Fuchs C, Janthur M, Hewicker-Trautwein M & Nolte I (2001) Comparison of the sensitivity of different diagnostic tests for pancreatitis in cats. JVIM 15 (4), 329-333. PubMed
• Simpson, K W (2001) The emergence of feline pancreatitis JVIM 15 (4), 327-328. PubMed
• Swift N C, Marks S L, MacLachlan N J, Norris C R (2000) Evaluation of serum feline trypsin-like immunoreactivity for the diagnosis of pancreatitis in cats. JAVMA 217, 37-42. PubMed
• Zhao P, Tu J, Martens A et al (1998) Radiologic investigations and pathologic results of experimental chronic pancreatitis in cats. Acad Radiol 5, 850-856. PubMed
• Bruner J M, Steiner J M, Williams D A, Van Alstine W G, Blevins W (1997) High feline trypsin-like immunoreactivity in a cat with pancreatitis and hepatic lipidosis. JAVMA 210, 1757-1760. PubMed
• Steiner J M & Williams D A (1997) Feline pancreatitis. Cont Educ Pract Vet 19, 590-602.
• Hines B L, Salisbury S K, Jakovljevic S & DeNicola D B (1996) Pancreatic pseudocyst associated with chronic-active necrotising pancreatitis in a cat. JAAHA 32, 147-152. PubMed
• Weiss D J, Gagne J M & Armstrong P J (1996) Relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis and nephritis in cats. JAVMA 209, 1114-1116. PubMed
• Akol K G, Washabau R J, Saunders H M & Hendrick M J (1993) Acute pancreatitis in cats with hepatic lipidosis. J Vet Intern Med 7 (4), 205-209. PubMed
• Hill R C & Van Winkle T J (1992) Acute necrotising pancreatitis and acute suppurative pancreatitis in the cat; a retrospective study of 40 cases (1976-1989). JVIM 7, 25-33. PubMed

• Dr Phil Nicholls BVSc BSc PhD MRCVS MRCPath, Division of Veterinary and Biomedical Sciences, Murdoch University, Murdoch, WA 6150, Australia.
• Dr Kenneth Simpson BVM&S PhD, Dept of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.

Back to top
© Copyright Vetstream

FELIS DIS01109

---