Diseases of the Exocrine Pancreas
Inflammation involving the pancreas is termed pancreatitis. In cats, the cause of most cases of pancreatitis remains unknown. Some cases result from abdominal trauma, tumors, intestinal obstructions, infectious diseases such as FIP and toxoplasmosis, liver and gallbladder disease, and insecticide poisoning. Infiltration of the pancreas by inflammatory cells of the body can also cause this condition.
Signs of pancreatitis include weakness, loss of appetite, excessive salivation, vomiting, diarrhea, dehydration, and abdominal pain. In addition, repeat bouts of pancreatitis can damage the insulin-producing cells of the pancreas, resulting in clinical signs associated with diabetes mellitus. Another aftereffect of chronic pancreatitis in cats can be a condition known as exocrine pancreatic insufficiency. Characterized by the inability of the pancreas to produce proper amounts of pancreatic digestive enzymes, exocrine pancreatic insufficiency is accompanied by a marked increase in appetite (due to poor digestion of nutrients), chronic weight loss, and diarrhea. This loose stool often contains large amounts of fat, which may cause a greasy soiling of the haircoat in the hindend.
Pancreatitis is difficult to definitively diagnose in cats. Traditional elevations in levels of amylase and lipase, two pancreatic enzymes, are not seen as consistently in cats as in dogs with the disease. Radiography, ultrasonography, and endoscopy can be employed as alternate diagnostic methods, yet even the reliability of these procedures can be inconsistent, In most instances, diagnosis is based on clinical signs seen and by a biopsy of the pancreas. If exocrine pancreatic insufficiency is suspected, specialized laboratory tests will need to be performed on a series of stool samples in order to positively identify the condition.
Cats experiencing only a mild bout of pancreatic inflammation will often recover on withholding all food and water for at least 24 hours. When treating severe cases of pancreatitis, it is imperative that all food, water, and even oral medications be discontinued for at least 48 hours. Intravenous fluids will be required as well to- prevent dehydration during this time. Additionally, antibiotics, pain relievers, and medications designed to reduce pancreatic secretions are usually employed to prevent secondary complications. Certainly all underlying disease conditions contributing to the pancreatitis must be addressed as well.
On recovery, cats should be maintained on dietary rations that are low in calories and easily digestible to reduce the workload placed on the pancreas. For those cats that are overweight, increasing exercise levels and promoting weight loss will reduce their susceptibility to subsequent flare-ups. Finally, cats experiencing exocrine pancreatic insufficiency due to chronic bouts with this disease will require enzyme supplementation to their diet to ensure adequate digestion of foodstuffs takes place.
For more technical information, please see below:
Diseases of the Feline Exocrine Pancreas
Robert M. Hardy, DMV, M.S.,
Diseases of the feline exocrine pancreas are difficult to diagnose and treat. Although
the cat appears to be susceptible to the same spectrum of pancreatic diseases as the dog
(i.e., acute and chronic pancreatitis, exocrine pancreatic insufficiency, and pancreatic
neoplasia), these disorders are much more difficult to recognize in cats than in dogs.
Precise figures on the incidence of these diseases are not known. Published rates on
numbers of cats with pancreatic disease per 1,000 cats seen very from 1.51 to 4.6.
At necropsy, this figure increases to 35 per 1,000 feline necropsies. Most
published reports on feline pancreatic diseases indicate that the diagnosis is most often
made at exploratory surgery (rarely) or on the necropsy table (most often).
INFLAMMATORY PANCREATIC DISEASE
Inflammatory pancreatic disease may be characterized as acute or chronic, but this is more appropriate for pathologic studies and is not often clinically relevant. On a clinical basis, it is impossible to differentiate these two classes of pancreatitis without histologic confirmation. Chronic interstitial pancreatitis is the most frequent pathologic description in cats.
The etiopathogenesis of feline pancreatitis is poorly understood. Published reports identify five etiologic associations: (1) coexisting cholangitis/cholangiohepatitis, (2) pancreatic fluke infestation, (3) pancreatic trauma, (4) pancreatic involvement
with toxoplasmosis, and (5) feline herpesvirus infection. In most cats with pancreatitis, however, a cause is not identified.
Biliary tract disease coexists with pancreatitis in many reported cases of feline pancreatitis. Some researchers consider cholangitis to be frequently, if not always, present in cases of chronic interstitial pancreatitis. It is presumed that ascending bacterial infections of both the common bile duct and major pancreatic duct occur simultaneously. Since the major pancreatic duct and common bile duct enter the duodenum at a common papilla, this is plausible. Culture of bile has only been reported
in two cases. Cultures were negative in one cat that had received systemic antibiotics prior to culture and 'positive for Escherichia coli in a second cat that had not had prior antibiotic therapy. It is also possible that cholangiohepatitis precedes
the onset of pancreatitis and may be responsible for its initiation. Retrograde lymph flow may occur from the extrahepatic biliary system into pancreatic lymphatics, carrying bile acids to the pancreas, which are capable of initiating acute pancreatitis.
The pancreatic trematode Eurytrema procyonis has been identified within the pancreatic ducts of cats from a number of
areas around the United States (New Jersey, Kentucky, Missouri, and the Ohio River Valley). Chronic infestations lead to severe pancreatic ductular and acinar fibrosis. Clinical signs relative to pancreatitis or exocrine insufficiency have not been reported, however. The cat liver fluke Amphimerus pseudofelineus has been associaed with chronic cholangitis and chronic pancreatitis (pancreatic cirrhosis) in a cat. Flukes were identified within hepatic and pancreatic cysts.
Several reports of traumatic acute pancreatitis in cats have appeared. All reported cases have been uniformly fatal, having a clinical course similar to hemorrhagic pancreatitis in dogs.
Unlike dogs, cats do not appear to be predisposed to the development of pancreatitis in association with high fat meals or the administration of drugs, particularly glucocorticoids. In addition, there does not appear to be an association between obesity and the onset of pancreatitis in cats, as there is in dogs. In spite of the aforementioned causes for feline pancreatitis, in most cases, a cause is never identified.
The pathogenesis of pancreatitis in cats is generally insidious and much less severe than in dogs, and it rarely progresses to death of the animal. In most published cases, the diagnosis was established at necropsy and the pancreatitis was generally subclinical and unsuspected. Important exceptions are (1) the rare cases of traumatic acute pancreatitis, in which mortality is high; (2) cats with cholangitis /cholangiohepatitis, in which liver disease is usually more severe than the pancreatic disease; (3) cats with obstructive jaundice secondary to common bile duct occlusion from pancreatic fibrosis and (4) cats that develop diabetes mellitus due to extensive islet cell destruction during the inflammatory process. Approximately 20 percent of diabetic cats show evidence of chronic pancreatitis at necropsy. Clinical signs of active pancreatitis are rarely present.
No apparent age, sex, or breed predispositions exist for cats with pancr atitis. For cats with chronic pancreatitis, a mean age
at diagnosis is approximately 8 years, but cats may be initially diagnosed when as young as 5 weeks of age or as old as 25 years
Clinical signs are highly variable and usually nonspecific. Weight loss, depression, and anorexia are the most common signs, with vomiting, polyuria polydipsia, and diarrhea occurring less frequently. Vomiting was present in 13 of 30 cats in two large case studies. Polyuria and polydipsia were due either to coexisting diabetes mellitus or chronic renal disease.
Physical examination findings, much like historical signs, are usually nonspecific. Depression and dehydration are common. Icterus is present in cats with coexisting cholangitis or extrahepatic biliary obstruction. Abdominal pain is rarely documented, except in severe acute pancreatitis. Fever is uncommon. Occasionally, muffled heart and lung sounds are detected due to pleural effusions associated with more acute cases. Rarely, an abdominal effusion and hepatomegaly or splenornegaly may be detected during abdominal palpation. In cats with acute, or subacute pancreatitis, and traumatic pancreatitis, a painful
cranial abdominal mass may be palpated within 2 to 3 days following the injury.
The clinical and pathologic changes in experimentally induced feline pancreatitis have been described in a recent report.
Clinical signs included depression, fever, rare vomiting (a single episode in two of six cats), and mild tachycardia. Abdominal discomfort and palpable cranial abdominal masses were detected in all cats.
A rare clinical finding associated with chronic pancreatitis is systemic lipodystrophy. Cats present with multiple subcutaneous nodules that may drain an oily fluid out the skin. Disseminated areas of fat necrosis are responsible for this manifestation.
Establishing a diagnosis of pancreatitis in cats requires considerable clinical acumen, thorough case histories, complete
physical examinations, extensive laboratory and radiographic evaluations, skilled ultrasonographic examinations, and a good deal of luck. It is important to remember that cats with pancreatitis often have subtle or absent clinical signs; exploratory laparotomies or necropsies have been required for definitive diagnosis in many cases. The clinical detection of feline pancreatitis is expected to increase, however, as the techniques of abdominal ultrasonography become more widely used in veterinary medicine.
Laboratory and radiographic evaluations of cats with inflammatory pancreatic disease have been very limited. Where data
are available, they are highly variable in terms of helping establish a definitive diagnosis. This probably reflects the low-grade, chronic nature of most cases. In the few severe acute pancreatitis cases reported, there are limited hematologic, biochemical, and radiographic data. Of eight cats in which the packed red blood cell volumes were known, only one had a decreased
value; the others were normal. A mature neutrophilia, ranging from 22,000 to 50,000 white blood cells/microl was detected
in 11 of 22 cats in which hemograms were reported. In cats with experimentally induced pancreatitis, significant hematologic abnormalities were limited to mild, normocytic, normochromic regenerative anemias. No significant neutrophilia or left shift
An appreciation for a typical biochemical profile is equally difficult to discern from published case reports. Serum concentrations of the hepatic enzymes alanine transaminase and alkaline phosphatase and bilirubin are increased in some cats with pancreatitis. In many others with extensive lesions and in cats with experimentally induced pancreatitiS, however, these parameters are normal. The magnitude of rise in serum alanine transaminase concentration is usually one to three times the upper limit of normal. Serum alkaline phosphatase concentration also is generally mildly increased, ranging from 1.5 to 15
times normal. Serum bilirubin concentrations were increased in 8 of 21 cases, but the magnitude of rise was not generally reported. The cause of the hepatic abnormalities in cats with pancreatitis is variable. Most cats had concurrent cholangioliepatitis or extrahepatic bile duct compression. In others, the presence of inflammatory pancreatitis leads to a toxic hepatitis when toxic pancreatic enzymes are delivered via pancreatic veins or lymphatics to the liver.
Hyperglycemia is a frequent biochemical abnormality in cats with acute or chronic pancreatitis. Mild hypercholesterolemia
was noted in cats with experimentally induced pancreatitis. Hyperglycemia was reported in 20 of 28 cats with pancreatitis in which blood glucose determinations were made. Many of these cats were not persistently hyperglycemic or glucosuric; thus, the hyperglycemia was presumably due to stress or transient injury to ß cells during the episode of pancreatitis. In several overtly diabetic cats, signs associated with the diabetes mellitus were the reason the cat was initially examined. The pancreatic lesion was often not recognized until necropsy. In diabetic cats in which insulin requirements decline or cease entirely, chronic pancreatitis may coexist. Mild flareups of pancreatitis may transiently impair the cat's insulin responsiveness leading to relapse of insulindependent diabetes.
Renal function has been evaluated in a few cats with pancreatitis. In one study, six of seven cats that died or that were euthanatized had blood urea nitrogen concentrations of 85 mg/dl or greater. Primary renal disease was a major reason for the cats being evaluated, not the pancreatitis. Most of these cats showed evidence of chronic progressive renal disease at necropsy. Prerenal uremia may also occur in cats with pancreatitis in association with vomiting, diarrhea, and anorexia, all of which may produce varying degrees of dehydration.
Electrolyte abnormalities are common in cats with pancreatitis, especially hypokalemia and hypocalcemia. Mild hypocalcemia also occurred in cats with experimentally induced pancreatitis. The hypocalcemia is not severe enough to produce clinical
signs but aids in supporting the diagnosis.
Serum amylase and lipase concentrations are generally accepted as the biochemical tests most useful in the diagnosis of
canine pancreatitis. Unfortunately, very few data are available to substantiate their value in feline pancreatitis. This is usually because the disease is not suspected prior to necropsy and these tests have not been performed. It has been suggested that serum amylase concentrations in feline pancreatitis are normal to two times normal and serum lipase concentrations are normal to three times normal. Limited data from published cases support that statement; however, most cats with pancreatitis have
had normal values for serum amylase and/or lipase. When increases were seen, they were never greater than three times the upper limit of normal for the laboratory being used.
It is not certain whether there is a diagnostic advantage to determining either amylase or lipase. Reports indicate that either
may be elevated in clinical cases. In cats with experimentally induced pancreatitis, the serum lipase was significantly increased in all cats. Lipase concentrations were six times normal during the initial 12 to 24 hours postoperatively but fell to three times normal for the next 2 days and were two times baseline on days 4 through 7. Interestingly, serum amylase concentrations
were significantly decreased during the acute stages of illness.
Serum amylase concentration may be increased in cats with renal failure. In one survey of cats with primary renal failure,
serum amylase concentration was increased in 10 of 32 cats. Necropsies on 7 of the 10 cats found histopathologic lesions of mild lymphocytic pancreatitis in only one cat, suggesting that hyperamylasemia was due to uremia, not pancreatitis.
Exocrine pancreatic insufficiency was assessed in cats with experimentally induced pancreatitis using bentiromide. Absorption was delayed and peak values were less postoperatively than preoperatively; however, the differences were not significant
from baseline values.
When abdominal effusions have been identified by palpation, survey radiographs, or ultrasound in cats with pancreatitis, abdominocentesis yields fluid characteristic of a sterile exudate.
Abdominal and thoracic radiographs may be of value in the diagnosis of pancreatitis. The normal pancreas is not radiographically visable. In pancreatitis, displacement of adjacent organs in the upper right quadrant of the abdomen may occur. Additional radiographic abnormalities include blurring of visceral outlines and a mottled flaky density confined to the ventral mesogastrium. Slow spreading of inflammation to involve the entire ventral abdomen may occur. Dorsal or
dorsomedial displacement of the duodenum and corrugation and spasticity of the duodenal wall were findings considered nearly pathognomonic for traumatic pancreatitis in cats. Pleural effusions are occasionally seen in cats with severe pancreatitis.
The normal feline pancreas is usually not visible ultrasonographically. Ultrasound evaluation of the abdomen is extremely
useful for identification of cranial abdominal soft tissue masses in the region of the pancreas, pancreatic abscesses, and increased peritoneal fluid in some cats. In cats with experimentally induced pancreatitis, abdominal ultrasound detected increased soft tissue and fluid echodensities in the pancreatic and peripancreatic region. Survey abdominal radiographs in two of these cats detected a cranial abdominal mass and loss of abdominal detail.
In summary, a definitive diagnosis of pancreatitis in cats is difficult to make on the basis of clinical, biochemical, and radiographic data; in many cases, the diagnosis will be speculative at best. Exploratory surgery or necropsy findings have confirmed the diagnosis in most cases. However, the diagnosis of pancreatitis is strongly supported by the finding a palpable
or ultrasonographically identified cranial abdominal mass in association with peritoneal fluid accumulation, transient hyperglycemia, and mild hypocalcemia in a cat with signs of vomiting, depression, and anorexia.
Therapeutic efforts for cats with pancreatitis should be directed at reversing the etiology, when known, and at providing
general supportive and symptomatic care when indicated. For cats identified as having concurrent cholangiohepatitis and chronic pancreatitis, antibiotics, with or without glucocorticoids, may bring about improvement in the hepatic disease and
cause the pancreatic inflammation to subside. A liver biopsy should be performed prior to initiation of antibiotic therapy, so
that cultures (aerobic and anaerobic) can be taken of both hepatic tissue and bile. If common bile duct obstruction is present due to pancreatic fibrosis, bile patency must be restored -surgically. For cats that develop pancreatic abscess (usually
identified by abdominal ultrasonography), surgical drainage or pancreatectomy is required, followed by management for peritonitis.
Pancreatic fluke infestations can cause significant functional alterations in the pancreas. Even though clinical signs are rare, it
is advisable to treat affected cats to eliminate the flukes. Treatment with fenbendazole (Panacur; 30 mg/kg PO q24h) for 6 consecutive days resulted in negative fecal examinations in one reported case. The drug was continued for an additional 3
days after a negative fecal examination was obtained. For discussion of hepatobiliary flukes.
Therapy for cats with chronic pancreatitis that become diabetic should be directed toward managing the diabetes mellitus. Occasionally, such cats become non-insulin dependent, presumably because as pancreatic inflammation subsides, islet cell function improves.
General supportive care is indicated for cats with more acute pancreatitis, using guidelines recommended for dogs. Balanced polyionic isotonic rehydrating fluids, such as lactated Ringer's solution, should be administered in volumes sufficient to meet maintenance requirements, replace any deficits, and keep pace with ongoing losses. Because hypokalemia is a common
finding in cats with pancreatitis, supplementation is warranted based on the severity of the deficits. In rare cases of fulminant acute pancreatitis, whole blood transfusions or plasma infusions may be of benefit to replace depleted a2-macroglobulins, which remove circulating active proteases.
Beneficial effects from prophylactic antibiotics in feline pancreatitis have not been confirmed. Most cases are mild and uncomplicated by infection. In humans, antibiotics with the best spectrum against bacterial pathogens identified in pancreatitis are clindamycin, metronidazole, tobramycin, and ciprofloxacin. Antibiotics considered slightly less effective include
cefotaxime, ceftazidime, netilimicin, rifampin, and trimethoprim-sulfa.
Food and water should be withheld during the acute vomiting state, as with other nonspecific gastroenteritides. Gradual introduction of a low-fat diet is indicated once signs of vomiting subside for 24 to 48 hours. Small frequent feedings are preferable to single large meals. Enteral support for persistently anorectic cats may be provided by a surgically placed jejunostomy tube in which a highly digestible enteral diet can be administered.