Pancreatitis—Dogs

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Pancreatitis—Dogs

 

Inflammation of the pancreas most often of unknown cause(s). Acute pancreatitis—inflammation of the pancreas that occurs abruptly with little or no permanent pathologic change. Chronic pancreatitis—continuing inflammatory disease that is accompanied by irreversible morphologic change such as fibrosis and atrophy.

 

PATHOPHYSIOLOGY

Inflammation of the pancreas most often of unknown cause(s). Acute pancreatitis—inflammation of the pancreas that occurs abruptly with little or no permanent pathologic change. Chronic pancreatitis—continuing inflammatory disease that is accompanied by irreversible morphologic change such as fibrosis and atrophy.

 

SYSTEMS AFFECTED

Gastrointestinal—altered GI motility (ileus) due to regional chemical peritonitis; local or generalized peritonitis due to enhanced vascular permeability.

Hepatobiliary—lesions due to shock, pancreatic enzyme injury, inflammatory cellular infiltrates, hepatic lipidosis, and intra/extrahepatic cholestasis.

Respiratory—pulmonary edema or pleural effusion; adult respiratory distress syndrome is an uncommon but potentially fatal sequela with systemic complications.

Cardiovascular—cardiac arrhythmias may result from release of myocardial depressant factor.

Hematologic—activation of the coagulation cascade and systemic consumptive coagulopathy (DIC) occur.

 

GENETICS

Possible genetic basis in miniature schnauzers where select mutations in the SPINK 1 gene may confer increased susceptibility.

 

INCIDENCE/PREVALENCE

  • True prevalence is unknown but a relatively common clinical disorder.
  • Up to 1% of normal dogs may have histologic evidence of pancreatitis.

 

GEOGRAPHIC DISTRIBUTION

Worldwide

 

SIGNALMENT

Species

Dog of any age

 

Breed Predilections

  • Miniature schnauzer
  • Yorkshire terrier
  • Cocker spaniel

 

Mean Age and Range

Acute pancreatitis is most common in middle-aged and older (> 7 years) dogs; mean age at presentation is 6.5 years.

 

Predominant Sex

Female

 

SIGNS

General Comments

Predominantly GI tract signs that are non-localizing and abdominal pain. Dogs with chronic pancreatitis may not exhibit abdominal pain.

 

Historical Findings

  • Lethargy/anorexia
  • Vomiting
  • Weakness
  • Abdominal pain
  • Diarrhea—small or large bowel type

 

Physical Findings

  • Severe lethargy.
  • Dehydration—common; due to GI losses.
  • Abdominal pain—may adopt a “prayer position” and/or resist abdominal palpation.
  • Mass lesions may be palpable.
  • Fever—common with more severe acute pancreatitis.
  • Less common systemic abnormalities include respiratory distress, bleeding disorders, and cardiac arrhythmias.

 

CAUSES

Etiology is most often unknown; possibilities include:

  • Nutritional factors (e.g., dietary indiscretion, hyperlipoproteinemia)
  • Pancreatic trauma/ischemia
  • Duodenal reflux
  • Drugs/toxins (see “Contraindications”)
  • Pancreatic duct obstruction
  • Hypercalcemia
  • Infectious agents—babesiosis
  • Nutrition—excessive lean body mass is associated with ANP

 

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS

  • Etiology is most often unknown; possibilities include:
  • Nutritional factors (e.g., dietary indiscretion, hyperlipoproteinemia)
  • Pancreatic trauma/ischemia
  • Duodenal reflux
  • Drugs/toxins (see “Contraindications”)
  • Pancreatic duct obstruction
  • Hypercalcemia
  • Infectious agents—babesiosis

 

CBC/BIOCHEMISTRY/URINALYSIS

  • CBC—acute pancreatitis often associated with hemoconcentration with increased PCV, leukocytosis with a left shift, and toxic neutrophils with severe inflammation; thrombocytopenia.
  • Serum biochemistries—often show prerenal azotemia; liver enzyme activities (ALT, ALP) are often increased because of hepatic ischemia or exposure to pancreatic toxins; hyperbilirubinemia with intra/extrahepatic biliary obstruction; electrolyte abnormalities associated with vomiting; hyperglycemia with necrotizing pancreatitis due to hyperglucagonemia; hypoalbuminemia; hypercholesterolemia and hypertriglyceridemia are common.
  • Urinalysis—increased urine SG associated with dehydration. Urinalysis may show evidence of proteinuria or may be unremarkable.

 

OTHER LABORATORY TESTS

  • CBC—acute pancreatitis often associated with hemoconcentration with increased PCV, leukocytosis with a left shift, and toxic neutrophils with severe inflammation; thrombocytopenia.
  • Serum biochemistries—often show prerenal azotemia; liver enzyme activities (ALT, ALP) are often increased because of hepatic ischemia or exposure to pancreatic toxins; hyperbilirubinemia with intra/extrahepatic biliary obstruction; electrolyte abnormalities associated with vomiting; hyperglycemia with necrotizing pancreatitis due to hyperglucagonemia; hypoalbuminemia; hypercholesterolemia and hypertriglyceridemia are common.
  • Urinalysis—increased urine SG associated with dehydration. Urinalysis may show evidence of proteinuria or may be unremarkable.

 

IMAGING

  • CBC—acute pancreatitis often associated with hemoconcentration with increased PCV, leukocytosis with a left shift, and toxic neutrophils with severe inflammation; thrombocytopenia.
  • Serum biochemistries—often show prerenal azotemia; liver enzyme activities (ALT, ALP) are often increased because of hepatic ischemia or exposure to pancreatic toxins; hyperbilirubinemia with intra/extrahepatic biliary obstruction; electrolyte abnormalities associated with vomiting; hyperglycemia with necrotizing pancreatitis due to hyperglucagonemia; hypoalbuminemia; hypercholesterolemia and hypertriglyceridemia are common.
  • Urinalysis—increased urine SG associated with dehydration. Urinalysis may show evidence of proteinuria or may be unremarkable.

 

DIAGNOSTIC PROCEDURES

  • Ultrasound-guided needle-aspiration biopsy may confirm inflammation (cytology), abscess, or cyst.
  • Laparoscopy with pancreatic biopsy forceps for histologic diagnosis.
  • Histopathologic evaluation may miss focal or segmental pancreatic inflammation; thus, this diagnostic tool must be interpreted with caution.

 

PATHOLOGIC FINDINGS

  • Gross findings (acute pancreatitis)—mild swelling with edematous pancreatitis; grayish yellow areas of pancreatic necrosis with varying amounts of hemorrhage with necrotizing pancreatitis.
  • Gross findings (chronic pancreatitis)—pancreas is reduced in size, firm, gray, and irregular; may contain extensive adhesions to surrounding viscera.
  • Microscopic changes (acute pancreatitis)—include edema, parenchymal necrosis, hemorrhage, and neutrophilic cellular infiltrate with acute lesions.
  • Microscopic changes (chronic pancreatitis)—pancreatic fibrosis around ducts, ductal epithelial hyperplasia, atrophy, and mononuclear cellular infiltrate.

 

TREATMENT

APPROPRIATE HEALTH CARE

Inpatient medical management most often required.

Aggressive IV fluid therapy.

Fluid therapy goals—correct hypovolemia and maintain pancreatic microcirculation.

A balanced electrolyte solution such as lactated Ringer’s solution (LRS) is the first-choice rehydration fluid.

Correct initial dehydration (mL = % dehydration × weight in kg × 1,000) and give over 4–6 hours.

May need colloids (oxyglobin, hetastarch) to improve pancreatic circulatory needs and prevent ischemia.

Following replacement of deficits, give additional fluids to match maintenance requirements (2.5 × weight in kg) and ongoing losses (estimated).

Potassium chloride (KCl) supplementation usually needed because of potassium loss in the vomitus; base potassium supplementation on measured serum levels (use 20 mEq of KCl/L of IV fluid if serum potassium levels are not known; do not administer faster than 0.5 mEq/kg/h).

 

ACTIVITY

Restrict

 

DIET

Continue to feed orally unless vomiting is intractable; feeding maintains intestinal epithelial integrity and minimizes bacterial translocation.

Initiate enteral feeding via esophagostomy, gastrostomy enteral device, or nasoesophageal tube placement.

NPO in animals with persistent vomiting for the shortest time possible; when there has been no vomiting for 12 hours, offer small volumes of water; if tolerated, begin small, frequent feedings of a carbohydrate (e.g., boiled rice); gradually introduce a protein source of high biologic value such as cottage cheese or lean meat.

Avoid high-protein and high-fat diets and use fat-restricted low-residue diets.

CLIENT EDUCATION

  • Discuss the need for extended hospitalization.
  • Discuss the expense of diagnosis and treatment.
  • Discuss possible short-term and long-term complications.

 

SURGICAL CONSIDERATIONS

  • May need surgery to remove pseudocysts, abscesses, or devitalized tissue seen with necrotizing pancreatitis.
  • May need laparotomy and pancreatic biopsy to confirm pancreatitis and/or rule out other, nonpancreatic diseases.
  • Extrahepatic biliary obstruction from pancreatitis requires surgical correction.

 

PREVENTION/AVOIDANCE

  • Weight reduction if obese.
  • Avoid high-fat diets.
  • Avoid drugs that may precipitate disease

 

POSSIBLE COMPLICATIONS

  • Failed response to supportive therapy.
  • Life-threatening associated conditions such as EPI, diabetes mellitus, and hepatic lipidosis.
  • Progression of acute pancreatitis to chronic pancreatitis.

 

MISCELLANEOUS

ASSOCIATED CONDITIONS

Life-Threatening

  • Pulmonary edema (e.g., adult respiratory distress syndrome)
  • Cardiac arrhythmias
  • Peritonitis
  • DIC

 

Non-Life-Threatening

  • Diabetes mellitus
  • EPI
  • Chronic pancreatitis

 

ABBREVIATIONS

ALP = alkaline phosphatase

ALT = alanine aminotransferase

ANP = acute necrotizing pancreatitis

DIC = disseminated intravascular coagulation

EHBO = extrahepatic biliary obstruction

EPI = exocrine pancreatic insufficiency

GI = gastrointestinal

IBD = inflammatory bowel disease

NPO = nothing per os

 

Visit your veterinarian as early recognition, diagnosis, and treatment are essential.

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