PANCREATIC ULTRASONOGRAPHY IN DOGS WITH EXPERIMENTALLY INDUCED ACUTE PANCREATITIS*

Two-dimensional ultrasonography was evaluated as an imaging modality in experimentally induced, acute pancreatitis in six dogs. Ultrasonic scans were performed once daily for one week following the induction of pancreatitis. Pancreatitis. Pancreatic inflammation, characterized by the development of nonhomogeneous masses and loss of echodensity in the pancreatic region, was consitently observed in all dogs. The results suggest that pancreatic ultrasonography may be a valuable technique for evaluating dogs with spontaneously occurring, acute pancreatitis.     

Serum values of amylase and pancreatic lipase in healthy mature dogs and dogs with experimental pancreatitis

Serum values of amylase and pancreatic lipase were determined by the iodometric and the turbidimetric methods, respectively, in 44 mature healthy dogs and in 8 dogs with experimentally induced pancreatitis (plus 1 sham-operated control). Serum value of amylase in mature healthy dogs varied from 250 to 1,500 Caraway units/dl and that of pancreatic lipase varied from 0 to 50 IU/L. Maximal serum values of amylase and pancreatic lipase in the dogs with experimentally induced pancreatitis varied from 4,540 to 14,000 Caraway units/dl and 325 to 810 IU/L, respectively. Following pancreatic damage, serum values of amylase and pancreatic lipase increased rapidly in the 8 dogs and ran parallel to each other in 6 of the 8 dogs studied. However, the serum value of amylase returned to within normal range earlier than the serum value of pancreatic lipase in 2 dogs; the reverse was true in 2 other dogs.     

Serum pancreatic polypeptide and amylase concentrations in dogs with experimentally induced acute pancreatitis

Serum concentrations of immunoreactive pancreatic polypeptide (IPP) were measured serially for 7 days after experimental induction of acute hemorrhagic pancreatitis in dogs by infusion of oleic acid into the pancreatic duct. The mean serum IPP concentrations in dogs with pancreatitis were increased significantly (P = 0.013) for 96 hours after induction of pancreatitis. Providing food at 108 hours resulted in significant increases (P = 0.032) in mean serum IPP concentrations in sham-operated control dogs compared with dogs with induced pancreatitis. This was attributed to cephalic-phase release of IPP due to a conditioned response that resulted from feeding immediately after each blood sampling. Mean serum IPP concentrations returned to base line more quickly than did mean serum amylase concentrations in dogs with pancreatitis.     

Chronic pancreatitis in dogs: A retrospective study of clinical,clinicopathological, and histopathological findings in 61 cases

The objective of this study was to characterize the clinical, clinicopathological, and histopathological findings of dogs with chronic pancreatitis. The necropsy database at Texas A&M University was searched for reports of dogs with histological evidence of chronic pancreatitis defined as irreversible histologic changes of the pancreas (i.e. fibrosis or atrophy). A reference necropsy population of 100 randomly selected dogs was used for signalment and concurrent disease comparisons. Cases were categorized as clinical or incidental chronic pancreatitis based on the presence of vomiting, decreased appetite, or both vs. neither of these signs. All archived pancreas samples were scored histologically using a published scoring system.Sixty-one dogs with chronic pancreatitis were included. The most frequent clinical signs were lethargy, decreased appetite, vomiting, and diarrhea. Compared to the reference necropsy population, chronic pancreatitis cases were more likely to be older, neutered, of the non-sporting/toy breed group, and to have concurrent endocrine, hepatobiliary, or neurological disease. Clinical cases had significantly higher histological scores for pancreatic necrosis and peripancreatic fat necrosis, and were significantly more likely to have hepatobiliary or endocrine disease as well as increased liver enzyme activities, or elevated cholesterol and bilirubin concentrations. In conclusion, clinical disease resulting from chronic pancreatitis might be related to the presence of pancreatic necrosis and pancreatic fat necrosis. The signalment, presentation, and concurrent diseases of dogs with chronic pancreatitis are similar to those previously reported for dogs with acute pancreatitis.     

Rapid turbidimetric determination of serum pancreatic lipase in the dog

A rapid and highly reproducible turbidimetric method for the determination of serum pancreatic lipase activity in the dog is described. Values of 0 to 50 IU/L of serum were obtained in 35 healthy mature dogs, and the maximum values of 325 to 800 IU/L were observed in 8 dogs with induced pancreatitis.     

Effects of dexamethasone on pancreatic tissue and on serum amylase and lipase activities in dogs

The effects of dexamethasone on the pancreas and on pancreatic amylase and lipase activities were determined in clinically normal dogs and in dogs with neurologic disease. Dexamethasone increased serum lipase activity without any histologic damage to the pancreas in either group of dogs. It decreased serum amylase activity in the normal dogs and had a variable effect in dogs with neurologic disease, with or without confirmed pancreatitis. It was suggested that high serum lipase activity in dexamethasone-treated dogs may not be attributable to pancreatitis and that the reasons are still unknown. It was concluded that high serum lipase activity is an unreliable basis for diagnosis of pancreatitis in dogs treated with dexamethasone. The data allowed no conclusion about an additive effect of dexamethasone and neurologic disease causing pancreatitis.     

Serum Pancreatic Lipase Immunoreactivity Concentrations in Dogs Treated with Potassium Bromide and/or Phenobarbital

Potassium bromide, phenobarbital, or a combination of both is commonly used in the treatment of canine epilepsy. Several cases of clinical pancreatitis have been reported in dogs after treatment with potassium bromide, but the risk of elevated serum canine pancreatic lipase immunoreactivity concentrations in dogs treated with potassium bromide and/or phenobarbital has not previously been evaluated in a large group of dogs. This study suggests an increased risk for elevated serum canine pancreatic lipase immunoreactivity concentrations and possibly pancreatitis in dogs treated with potassium bromide or phenobarbital alone or in combination.     

CONTRAST‐ENHANCED ULTRASONOGRAPHY OF THE PANCREAS IN HEALTHY DOGS AND IN DOGS WITH ACUTE PANCREATITIS

Pancreatitis is the most frequent disease affecting the exocrine pancreas in dogs and reliable diagnostic techniques for predicting fatal complications are lacking. Contrast‐enhanced ultrasound (CEUS) improves detection of tissue perfusion as well as organ lesion vascular pattern. Objectives of this prospective case control study were to compare perfusion characteristics and enhancement patterns of the pancreas in healthy dogs and dogs with pancreatitis using CEUS. Ten healthy dogs and eight dogs with pancreatitis were selected based on physical examination, abdominal ultrasound, and blood analysis findings. A CEUS study of the pancreas was performed for each dog and two observers who were aware of clinical status used advanced ultrasound quantification software to analyze time‐intensity curves. Perfusion patterns were compared between healthy and affected dogs. In dogs with acute pancreatitis, mean pixel and peak intensity of the pancreatic parenchyma was significantly higher than that of normal dogs (P = 0.05) in between 6 and 60 s (P = <0.0001–0.046). This corresponds to a 311% increase in mean pixel intensity in dogs with acute pancreatitis compared to healthy dogs. Wash‐in rates were greater and had a consistently steeper slope to peak in dogs with pancreatitis as opposed to healthy dogs. All dogs with pancreatitis showed a decrease in pixel intensity 10–15 days after the initial examination (P = 0.011) and their times to peak values were prolonged compared to the initial exam. Findings from the current study supported the use of CEUS for diagnosing pancreatitis, pancreatic necrosis, and disease monitoring following therapy in dogs.     

Use of laparoscopy for diagnosing experimentally induced acute pancreatitis in dogs

Diagnosis of acute pancreatitis in dogs remains a significant challenge despite the development of advanced diagnostic methodologies. Visual inspection and pancreas biopsy using laparoscopy are generally considered to be procedures free of complications when conducted on healthy animals. However, the usefulness of laparoscopy for diagnosing acute pancreatitis has not been assessed. In the present study, the efficacy of laparoscopy for diagnosing acute pancreatitis in dogs was evaluated in animals with experimentally induced acute pancreatitis. Gross appearance of the pancreatic area was examined by laparoscopy to survey for the presence of edema, adhesions, effusion, pseudocysts, hemorrhage, and fat necrosis. Laparoscopic biopsy was performed and the histopathologic results were compared to those of pancreatic samples obtained during necropsy. The correlation between laparoscopy and histopathologic findings of the pancreas was evaluated. The presence of adhesions, effusion, and hemorrhage in the pancreatic area observed by laparoscopy significantly correlated with the histopathologic results (p < 0.05). There was no significant relationship between the histopathologic and laparoscopic biopsy findings. Results of this study suggested that laparoscopic evaluation of gross lesions has clinical significance although the laparoscopic biopsy technique has some limitations. This method combined with additional diagnostic tools can be effective for diagnosing acute pancreatitis in dogs.     

A pilot study evaluating changes in pancreatic lipase immunoreactivity concentrations in canines treated with L-asparaginase (ASNase), vincristine, or both for lymphoma

L-asparaginase (ASNase) is a common chemotherapy agent for the treatment of lymphoid malignancies. L-asparaginase has been reported to cause clinical pancreatitis in both humans and canines. Canine pancreatic lipase immunoreactivity (cPLI) is now a common diagnostic tool for evaluating pancreatitis in dogs. A total of 52 dogs were enrolled into this study. Canine pancreatic lipase immunoreactivity (cPLI) concentrations were evaluated before and after administration of ASNase, vincristine, or both. All dogs enrolled in the study were evaluated for signs compatible with clinical pancreatitis. No dogs receiving ASNase alone showed evidence of clinical pancreatitis after administration. Also, there was no statistically significant change in cPLI concentrations before or after treatment. Fourteen percent of dogs that received both vincristine and ASNase concurrently had elevated concentrations of cPLI after treatment. Of the 11 dogs with clinical signs compatible with pancreatitis after any chemotherapy treatment, no dog had a cPLI concentration > 400 μg/dL. In conclusion, ASNase did not cause clinical pancreatitis in this cohort of dogs but larger sample sizes are required to further validate this data.     

Pancreatic Degenerative Atrophy and Chronic Pancreatitis in Dogs a Comparative Study of 60 Cases

During the years 1977–1980 60 cases of non-neoplastic chronic exocrine pancreatic disease in dogs were investigated clinically and pathologically. The disorders were clinically divided into pancreatic degenerative atrophy (PDA) and chronic pancreatitis. Fifty dogs had PDA and 45 of them were German shepherd dogs. The PDA cases formed both clinically and pathologically a homogeneous group except for 1 case. All the dogs had maldigestion and protease activity was absent from the faeces. General inanition and highly atrophic pancreas were the most typical macroscopic findings. Histologically the exocrine pancreas contained atypical acinar tissue and mononuclear cell infiltrations. Five of the dogs died spontaneously, 4 of them had intestinal torsion and 1 had paralytic ileus.There were 10 dogs with chronic pancreatitis. This group was rather heterogeneous both clinically and pathologically. The pancreas was slightly enlarged and the consistency was firm. The histologic picture was one of fibrous tissue proliferation and inflammatory cell infiltrations in the interstitium. The dogs nutritional state as well as faecal protease activity were normal.     

Model of chronic pancreatitis in the dog

A model of chronic pancreatitis was developed and characterized in the dog. Pancreatitis was produced by infusion of oleic acid through a cannula in the accessory pancreatic duct. Biochemical changes included early and marked increases in serum amylase and lipase activities which returned to base line within 3 weeks, at which time the dogs were clinically normal. In dogs euthanatized within 2 weeks, pathologic changes included massive necrosis and hemorrhage, cystic spaces filled with fluid, and abscesses. Histologic features revealed acute exudative pancreatitis with pancreatic atrophy and fibrosis. In dogs killed between weeks 3 to 12, changes included: marked atrophy with remaining acini surrounded by remnants consisting of collapsed stroma, blood vessels, and pancreatic ducts; marked coarse fibrosis with scattered inflammatory cells and occasional acinar tissue; and large irregular pseudocysts.     

Dilation of the pancreatic duct: An ultrasonographic finding in acute pancreatitis

Dilation of the pancreatic duct in two dogs with acute pancreatitis was identified using ultrasonography. This sign supported the diagnosis of pancreatitis. However, reference to the human medical literature indicates that dilation of the pancreatic duct may occur with a variety of conditions, and should be considered a potentially non-specific finding in dogs.     

Autoantibodies to pancreatic islet cells in canine diabetes mellitus

Indirect immunofluorescence on normal canine pancreatic tissue fixed in Bouin's solution was used to detect islet cell antibodies in dogs with diabetes mellitus, other endocrine diseases, and pancreatitis. 18 of 25 dogs with diabetes mellitus alone, 2 of 8 dogs with diabetes mellitus and concurrent pancreatitis, and 2 of 2 dogs with diabetes mellitus and concurrent pancreatic exocrine insufficiency were positive for autoantibody. 2 of 12 dogs with hypoadrenocorticism, 3 of 6 dogs with hyperadrenocorticism, 6 of 28 dogs with hypothyroidism and one of 19 dogs with pancreatitis alone were also antibody positive. None of 20 healthy dogs or 20 dogs with disorders other than those of the pancreas or endocrine organs were antibody positive. Islet cell antibodies were demonstrated in dogs with diabetes mellitus and other endocrine disorders. The possibility of autoimmune involvement in the development of diabetes mellitus in the dog should be considered.     

Characteristics and outcomes in surgical management of severe acute pancreatitis: 37 dogs (2001–2007)

Objective – Describe clinical characteristics and outcomes associated with canine patients undergoing surgical intervention for treatment of acute pancreatitis.
Design – Retrospective outcome study from 2001 to 2007.
Animals – Thirty-seven dogs.
Interventions – None.
Measurements and Main Results – The following data were collected for dogs who underwent surgical intervention in the course of treatment for severe acute pancreatitis: preoperative clinicopathologic and physical data, ultrasonographic findings, surgical procedure detail, histopathologic findings, and transfusion requirements. The survival rate was 80.8% in dogs with extrahepatic biliary obstruction, 64.3% in dogs undergoing necrosectomy, and 40.6% with pancreatic abscess. Overall survival was 63.6%. Surgical complications included intraoperative and postoperative hemorrhage in 12 dogs, postoperative development of diabetes mellitus in 3 dogs, exocrine pancreatic insufficiency in 1 dog, and bacterial peritonitis in 2 dogs.
Conclusion – Surgical intervention and aggressive postoperative care may be pursued in select dogs with severe acute pancreatitis. In dogs with extrahepatic biliary obstruction secondary to acute pancreatitis, surgical intervention may be associated with a good prognosis whereas dogs with pancreatic abscess formation may have a more guarded prognosis.     

Diseased dogs isoamylases in clinically normal and diseased dogs

Isoamylases in normal canine sera were separated on cellulose acetate membranes using a discontinuous buffer system without EDTA. Four peaks of amylase activity were present in 17 of 24 sera. Normal values were established. The majority of activity was present in Peak 4 (cathodal isoamylase). Tissue extracts of pancreas, duodenum, kidney, lung, testis, spleen and uterus-ovaries contained Peak 4 isoamylase. Liver and salivary gland lacked all isoamylase activity. Pancreas contained Peak 3 in addition to Peak 4 isoamylase. A tissue origin for Peaks 1 and 2 was not identified. An overall lack of resolution resulted from the inclusion of EDTA in the electrophoresis buffer system. This may account for previous findings suggesting that pancreatic amylase is not present in normal canine serum. An increase in the Peak 3 isoamylase was present in dogs with pancreatitis while dogs with pancreatic atrophy had a decrease in all isoamylases. Total amylase activity was significantly (p < 0.05) decreased in dogs with pancreatic atrophy.     

Subclinical exocrine pancreatic insufficiency in dogs

OBJECTIVE: To study progression of autoimmune-mediated atrophic lymphocytic pancreatitis from the subclinical to the clinical phase (exocrine pancreatic insufficiency [EPI]) and determine whether progression of the disease could be halted by treatment with immunosuppressive drugs. DESIGN: Randomized controlled trial. ANIMALS: 20 dogs with subclinical EPI. PROCEDURE: Diagnosis of subclinical EPI was determined on the basis of repeatedly low serum trypsin like-immunoreactivity (TLI) in dogs with no signs of EPI. Laparotomy was performed on 12 dogs with partial acinar atrophy and atrophic lymphocytic pancreatitis. A treatment group (7 dogs) received an immunosuppressive drug (azathioprine) for 9 to 18 months, and a nontreatment group (13) received no medication. RESULTS: During the subclinical phase, serum TLI was repeatedly low (< 5.0 microg/L). Although a few dogs had nonspecific gastrointestinal tract signs, they did not need diet supplementation with enzymes. While receiving immunosuppressive medication, treated dogs had no clinical signs of EPI, but within 2 to 6 months after treatment was stopped, 2 dogs had signs of EPI, and diet supplementation with enzymes was started. Five of the 13 untreated dogs needed diet supplementation with enzymes within 6 to 46 months. During follow-up of 1 to 6 years, 3 of the 7 treated dogs and 8 of the 13 untreated dogs did not need continuous diet supplementation with enzymes. CONCLUSIONS AND CLINICAL RELEVANCE: Progression of atrophic lymphocytic pancreatitis varied widely. The subclinical phase may last for years and sometimes for life. The value of early treatment with an immunosuppressive drug was questionable and, because of the slow natural progression of the disease, cannot be recommended.     

Exocrine pancreatic insufficiency as an end stage of pancreatitis in four dogs

Chronic pancreatitis is a common cause of exocrine pancreatic insufficiency (EPI) in humans and cats but is rarely recognised in dogs in which pancreatic acinar atrophy (PAA) is reportedly more common. This paper describes four dogs which developed EPI secondary to pancreatitis. Two of the dogs also had diabetes mellitus which developed before EPI. One diabetic dog had concurrent hyperadrenocorticism and was euthanased five months after presentation; the other diabetic dog died 48 months after diagnosis. The remaining dogs were alive 78 and 57 months after diagnosis. The number of affected dogs was comparable to the number of cases of presumed PAA seen over the same time period in the same institution. Chronic pancreatitis may be a more common cause of EPI in dogs than previously assumed and may be under-recognised because of difficulties in diagnosis. The relative importance of chronic pancreatitis as a cause of canine diabetes mellitus remains to be ascertained.     

Serum antiprotease concentrations in dogs with spontaneous and experimentally induced acute pancreatitis

A significant decline (P = 0.047) in serum antiprotease concentration was detected in dogs with experimentally induced acute pancreatitis. Decreased serum antiprotease concentrations, similar in magnitude to those documented in the experimental dogs, were present in dogs with spontaneous, acute pancreatitis. These findings suggest that significant amounts of proteolytic enzymes escape into the systemic circulation during acute pancreatitis in dogs. These circulating enzymes may be involved in the extrapancreatic complications of acute pancreatitis.     

Prednisone treatment alters the serum amylase and lipase activities in normal dogs without causing pancreatitis.

In order to test the hypothesis that treatment with glucocorticoids causes pancreatitis in dogs, 18 mongrel dogs were divided into three groups of six individuals, each group receiving prednisone at different doses orally or intramuscularly for two weeks. Two groups consisting of six dogs each served as controls. Treatment for two weeks with oral prednisone at 1.2 mg/kg body weight or at 4 mg/kg body weight daily decreased the serum amylase activities, but increased the serum lipase activities. Postmortem examinations revealed microscopic evidence of mild pancreatitis in only one dog given prednisone, that clinically appeared normal. It was concluded that daily doses of 4 mg prednisone/kg body weight or less given orally or intramuscularly for two weeks do not cause pancreatitis in dogs.