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.     

Effects of an anticholinergic and a corticosteroid on acute pancreatitis in experimental dogs

In a model developed to study acute pancreatitis in the dog, the disease process was comparable with the spontaneously occurring disease. Infusion of oleic acid into the accessory pancreatic duct induced, grossly and microscopically, acute hemorrhagic pancreatitis with pancreatic atrophy, fibrosis, fat necrosis, and edema. Clinical changes included persistent fever and tachycardia in all dogs and abdominal pain, vomiting, and diarrhea in most. Serum amylase and lipase activities increased markedly as did activities of alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase. Hematologic alterations included hemoconcentration (despite intensive fluid therapy) and leukocytosis due primarily to neutrophilia and monocytosis. Neither corticosteroid nor anticholinergic therapy begun 24 to 32 hours after oleic acid infusion altered the course of the disease. Dogs survived 8 days and appeared clinically normal when the study was terminated.     

Exocrine pancreatic atrophy in German Shepherd Dogs and Rough-coated Collies: an end result of lymphocytic pancreatitis

Previously published studies of the pathology of canine exocrine pancreatic insufficiency (EPI) have been based on morphological findings during the clinical phase of the disease, when atrophy of acinar parenchyma occurs. Recently, low serum trypsinlike immunoreactivity (TLI) concentration has been shown to precede clinical signs, making it possible to diagnose EPI prior to onset of the clinical disease. This study presents histological and ultrastructural findings of pancreatic biopsies from 11 German Shepherd Dogs and 2 Rough-coated Collies with subclinical EPI (SEPI). These findings were compared with those from dogs with clinical EPI (n = 11) and healthy control dogs (n = 5). Biopsied tissue from dogs with SEPI typically contained both normal and atrophied acinar parenchyma. The most significant finding was the marked lymphocytic infiltration, which was most prevalent at the border zone of affected and nonaffected parenchyma but had spread into the normal acinar tissue. Numerous intraacinar lymphocytes were found. Most of the lymphocytes were positive by immunostaining for CD3. In more advanced stages of destruction, the findings were characteristic of pancreatic acinar atrophy. In the atrophied parenchyma, the inflammatory reaction, if present, was less prominent. Ultrastructural changes were in accordance with those of the histological study showing infiltration of lymphocytes both in affected acini and in acini that revealed no obvious ultrastructural changes. Progressive degenerative changes of acinar cells were considered a nonspecific finding. Apoptotic death of acinar cells was occasionally found. The inflammatory reaction was clearly shown to precede the pancreatic acinar atrophy, and the findings suggested that lymphocytic pancreatitis leads to atrophy of the pancreas. The possibility that EPI is an immune-mediated disease in German Shepherd Dogs and Rough-coated Collies is discussed.     

Cellular and humoral immune responses in atrophic lymphocytic pancreatitis in German shepherd dogs and rough-coated collies

The most common cause for the clinical signs of exocrine pancreatic insufficiency (EPI) in dogs is pancreatic acinar atrophy (PAA). In the subclinical phase of EPI, before total atrophy occurs, exocrine pancreas is affected by infiltrative lymphocytic inflammation, which gradually leads to selective destruction and atrophy of the acinar tissue.Here, we analyzed the role of cell-mediated and humoral immune mechanisms in the pathogenesis of atrophic lymphocytic pancreatitis in German shepherd dogs and rough-coated collies. Pancreas biopsies and serum samples were obtained from 12 dogs with subclinical EPI (SEPI), 13 dogs with clinical EPI and 13 healthy control dogs.Immunohistochemical analysis showed that, in the subclinical phase, the majority of the infiltrating lymphocytes were T-cells with an almost equal number of CD4+ 'T-helper' and CD8+ 'cytotoxic' T-lymphocytes. The distribution of the two lymphocyte subsets was different. Typically, the CD4+ cells were present in large cellular infiltrates in the affected parenchyma, and the scattered CD8+ cells had infiltrated both the affected and the normal parenchyma. In sections where destruction of acinar parenchyma was present, the CD8+ T-cells were predominant. In cases of marked T-cell infiltration, CD79+ B-lymphocytes and plasma cells, and lysozyme-positive macrophages were also detected. Lymphoid follicle germinal centers with a majority of cells staining positively for CD79 were found. The lymphocytic infiltration in the totally atrophic tissue of dogs with clinical EPI was less prominent. Indirect immunofluorescence staining showed serum antibodies reacting weakly with pancreatic acinar cells in five out of nine dogs with subclinical and three out of 10 dogs with clinical EPI, but not in the control dogs.The results suggest that the tissue destruction is largely T-cell-mediated, although the presence of numerous B-lymphocytes and pancreas-specific antibodies in the sera of some dogs indicate that humoral mechanisms are also involved. In conclusion, this study suggests that the atrophic lymphocytic pancreatitis in German shepherds and rough-coated collies is an autoimmune disease.     

ENDOSCOPIC ULTRASONOGRAPHIC FINDINGS OF THE PANCREAS AFTER PANCREATIC DUCT LIGATION IN THE DOG

Endoscopic ultrasonographic evaluation and gray-scale histogram analysis of pancreatic atrophy after pancreatic duct ligation were performed in four normal adult dogs. Using endoscopic ultrasonography, markedly dilated pancreatic ducts were visualized, and the pancreas became gradually atrophied with a hyperechoic parenchyma. In gray-scale histogram analysis of the pancreas, mean brightness increased gradually until 8 weeks, then decreased temporally. Standard deviation of the histogram increased markedly and then fluctuated until the 4th week, after which the mean brightness and standard deviation became stable. At 4 weeks postoperatively, collapse of most pancreatic acinar structures were observed, and each atrophic lobule was associated with a significantly large amount of interstitial fibrous tissue at histopathology. At 12 weeks postoperatively, most exocrine tissue had decreased and was partly replaced by fibrous and fatty tissue. These changes of mean brightness and standard deviation reflected the histologic analysis. These findings indicated that endoscopic ultrasonography is a useful technique to image such atrophic disorders of the pancreas as chronic pancreatitis. Furthermore, gray-scale histogram analysis provides helpful information for ultrasonographic tissue characterization of the pancreas.     

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.     

Bile duct obstruction secondary to chronic pancreatitis in seven dogs

Seven icteric dogs were determined to have bile duct obstruction secondary to chronic pancreatitis. All dogs had histories of intermittent vomiting and diarrhea. Alkaline phosphatase and alanine aminotransferase activities and total bilirubin concentrations were markedly elevated. Diagnosis was based on exploratory laparotomy and histological examination. Each dog had a 3 to 10 cm mass in the body of the pancreas and obstruction of the common bile duct. Three dogs treated with pancreatectomy, gastrojejunostomy, and cholecystojejunostomy died within five weeks. Three dogs treated with conservative surgical procedures were alive at 8, 16, and 26 months postoperatively. One dog was euthanized because of suspected neoplasia. Hepatic enzyme activity and bilirubin levels decreased markedly in the surviving dogs. Histological examination of the pancreatic masses indicated chronic pancreatitis. Hepatic biopsies revealed evidence of cholestasis. Chronic pancreatitis should be included in the differential diagnoses of icterus, bile duct obstruction, and masses in the pancreas.     

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.     

Localization of pancreatic inflammation and necrosis in dogs

Few studies of the prevalence of histologic lesions of the exocrine pancreas in dogs have been reported, and none of them systematically evaluate the localization of these lesions. The purpose of this study was to describe the anatomic localization of pancreatic inflammation, necrosis, and fibrosis in dogs presented for postmortem examination. Seventy-three pancreata from dogs presented for postmortem examination were evaluated and investigated for the presence of suppurative inflammation (SI), pancreatic necrosis (PN), and lymphocytic inflammation (LI). Sections that showed evidence of SI, PN, or LI also were evaluated for pancreatic fibrosis (F). The tendency for a preferred localization for SI, PN, and LI was evaluated by chi-square analysis. A total of 47 pancreata with histologic evidence of pancreatitis (SI, PN, or LI; F alone was not considered evidence of pancreatitis) were identified. Twenty-four (51.1%) had SI, 23 (48.9%) had PN, and 34 (72.3%) had LI. Of the 47 dogs with SI, PN, or LI, 28 (59.6%) had F. The distribution of SI, PN, and LI between the right and the left limb of the pancreas and among the 5 anatomic regions was random, based on a goodness-of-fit test. We conclude that pancreatic inflammation tends to occur in discrete areas within the pancreas rather than diffusely throughout the whole organ. These findings suggest that a single biopsy is insufficient to exclude subclinical pancreatitis and that there is no preferred site for pancreatic biopsy collection unless gross lesions are apparent.     

CT angiographic changes in dogs with acute pancreatitis: A prospective longitudinal study

Computed tomographic angiography (CTA) has recently been shown to be a useful tool in the diagnosis of acute canine pancreatitis, the identification of pancreatic necrosis, and the detection of sequelae. Evidence of pancreatic necrosis on CTA has been shown to be correlated with a poorer outcome in both humans and dogs and early diagnosis and intervention may improve outcomes. In humans, pancreatic necrosis is typically evident on CTA within 48 h of clinical signs, thus, repeat CTA examinations are often performed to identify pancreatic necrosis that may not have been evident on CTA examinations performed early in the course of disease. Published information investigating the timing of CTA examinations and the use of serial CTA in dogs with acute pancreatitis is lacking. In this prospective, longitudinal study, CTA examinations were performed at the time of hospitalization and repeated 3‐5 days later in 11 dogs suffering from acute canine pancreatitis to determine if pancreatic necrosis or sequelae are under diagnosed on examinations performed at the time of hospitalization. Computed tomographic angiography studies were evaluated for changes in pancreatic size, pancreatic contrast enhancement, and peri‐pancreatic tissues and vessels. The only statistically significant difference between the initial and repeat CTA examinations was the improvement of fat stranding on the repeat CTA examinations (P < .045). Based on these results, CTA performed at the time of admission is likely adequate in the diagnosis and evaluation of dogs with acute pancreatitis. Repeat CTA examinations are unlikely to add additional information in the absence of worsening clinical signs.     

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.     

Increased canine pancreatic lipase immunoreactivity (cPLI) and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester (DGGR) lipase in dogs with evidence of portal hypertension and normal pancreatic histology: a pilot study

The clinical presentations of both liver disease and pancreatitis are nonspecific and overlapping, which may cause difficulty in diagnosis. In our retrospective pilot study, we assessed whether dogs with evidence of portal hypertension and absence of pancreatitis on pancreatic histology have increases in canine pancreatic lipase immunoreactivity (cPLI) and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester (DGGR) lipase. We included dogs that had been presented between 2008 and 2019 if they had normal pancreatic histology, histologically confirmed hepatopathy, and if canine pancreas-specific lipase (Spec cPL; Idexx) or DGGR lipase had been measured. Only dogs with portal hypertension were included. Six dogs fulfilled the inclusion criteria. Four of 6 and 2 of 6 dogs had Spec cPL and DGGR lipase exceeding the upper reference limit, respectively. From the 4 dogs with increased Spec cPL, 2 had concentrations of 200–400 µg/L and 2 had concentrations ≥ 400 µg/L. Our results suggest that canine portal hypertension might lead to increased Spec cPL and DGGR lipase values in the absence of pancreatitis on histology. Until more evidence in a larger number of dogs with portal hypertension is available, both tests should be interpreted cautiously in the presence of portal hypertension.     

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.     

Aflatoxicosis in nine dogs after exposure to contaminated commercial dog food.

The purpose of this study was to characterize light and electron microscopic findings from 9 dogs that had consumed aflatoxin-contaminated commercial dog food from recalled batches. Four dogs died and 5 were euthanized after signs of liver failure. Analysis of feed and liver samples confirmed exposure to aflatoxin. Of the 9 dogs, 8 had classic signs of liver failure, and 1 had signs of liver failure. Enlarged, pale yellow livers were seen macroscopically at necropsy in the dogs with subacute hepatopathy, and cirrhosis was noted in the dog with chronic hepatopathy. Histopathologic findings included hepatic lipidosis, portal fibroplasia, and biliary hyperplasia, which supported a diagnosis of subacute toxic hepatopathy in the 8 symptomatic animals. Marked lobular atrophy, bridging portal fibrosis, and regenerative hepatocellular nodules characterized the dog with chronic hepatopathy. Electron microscopy revealed marked hepatocellular lipid vacuolation and early fibroplasia in the dogs with acute hepatopathy and marked fibrosis and regeneration in the dog with chronic hepatopathy. Analysis of feed for aflatoxin consistently revealed high levels of aflatoxin B1 (range of 223-579 ppb), and hepatic tissue contained elevated levels of aflatoxin B1 metabolite M1 (0.6-4.4 ppb). Although dogs are not commonly affected by aflatoxicosis, they are highly susceptible and can present with classic signs of acute or chronic hepatopathy. Characteristic gross, histologic, and electron microscopic changes help pathologists determine a presumptive toxic insult. Detecting aflatoxins or their metabolites in feed or liver specimens can help confirm the diagnosis of aflatoxicosis.     

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.     

Characterization of chronic pancreatitis in English Cocker Spaniels

Background: Chronic pancreatitis (CP) is common in dogs. The cause is unknown. In humans, different causes of pancreatitis have histologically distinct appearances. The histopathologic lesions in English Cocker Spaniels (ECS) with CP were noted to be histologically different than those of other breeds with CP. Hypothesis: CP in ECS is distinct from CP in other breeds and is characterized by a duct destruction similar to what is observed in autoimmune CP of humans. Animals: Eight ECS and 9 other breeds with histologically confirmed CP recruited over an 8‐year period and 50 postmortem control dogs with CP. Methods: Clinical, clinicopathological, and ultrasonographic findings were recorded. Histological sections were compared with a normal dog and 59 dogs of other breeds with CP. Immunohistochemistry using anti‐CD3, anti‐CD79a, and anti‐cytokeratin antibodies was used to evaluate distribution and type of lymphocytic inflammation and appearance of pancreatic ducts. Results: Four male and 4 female ECS presented at a mean age of 7.2 years. Clinical signs were similar in ECS and other breeds. The pancreas was enlarged and hypoechoic in 4 ECS and 2 controls. Histopathology was characterized by interlobular and periductular fibrosis and inflammation in ECS compared with intralobular disease in most other breeds. Immunohistochemistry identified prominent anti‐CD3⁺ lymphocytic infiltrates around venules and ducts and a marked absence of interlobular ducts in ECS compared with mixed T‐cell infiltration and ductular hyperplasia in most other breeds with CP. Conclusions and Clinical Importance: CP in ECS is distinct from CP in other breeds and is notably duct destructive.     

Juvenile Pancreatic Atrophy in Greyhounds: 12 Cases (1995–2000)

Background: This study describes compound failure of the endocrine and exocrine pancreas in Greyhounds, a condition that has not been reported in the veterinary literature.
Objective: To describe the clinical and pathologic findings in 12 Greyhounds with juvenile pancreatic atrophy.
Animals: Ten Greyhounds presented for necropsy examination and 2 sibling Greyhounds presented for clinical evaluation before necropsy, all with a history of small-bowel diarrhea.
Procedures: Retrospective study of laboratory and pathologic findings in 12 Greyhounds, including serum trypsin-like immunoreactivity assays, oral glucose tolerance testing, and serum anti-insulin antibody concentrations.
Results: Gross pancreatic atrophy was found in all 12 dogs. Histopathologic lesions were found in both the endocrine and exocrine pancreas and included acinar cell apoptosis, zymogen granule loss, cytoplasmic clearing or vacuolar change, lobular atrophy, islet loss, and lymphocytic or lymphoplasmacytic pancreatitis. Antemortem test results on the 2 Greyhound puppies indicated concurrent exocrine pancreatic insufficiency (EPI) and insulin-dependent diabetes mellitus (IDDM).
Conclusions and Clinical Importance: Compound failure of the exocrine and endocrine pancreas is rarely reported in dogs and neither disease is well recognized in the Greyhound. This condition is of potential economic importance to the Greyhound racing industry.     

Computed Tomographic Angiography under Sedation in the Diagnosis of Suspected Canine Pancreatitis: A Pilot Study

Background

Computed tomography (CT) is highly accurate for diagnosing pancreatitis in humans. The diagnosis of pancreatitis in dogs is based on clinical signs, laboratory findings, and ultrasonographic (US) changes. There are, however, inherent limitations in relying on laboratory and ultrasound findings for the clinical diagnosis of pancreatitis in dogs.

Hypothesis/Objectives

We hypothesized that CT angiography would be a rapid and reliable method to confirm pancreatitis in dogs compared to ultrasonography. The aim was to describe the CT characteristics and compare them to ultrasound findings and correlate the CT appearance to the severity of the patients'' clinical course.

Animals

A prospective pilot case series; 10 dogs with pancreatitis were enrolled if the history, clinical signs, laboratory, and ultrasonographic findings were indicative of pancreatitis.

Methods

A 3‐phase angiographic CT was performed under sedation. Afterward, each dog had US‐guided aspirates of the pancreas collected and blood drawn for cPLi assay. Images were evaluated for portion of visible pancreas, pancreatic size and margin, pancreatic parenchyma, presence of peripancreatic changes and contrast enhancement pattern. The results were compared with outcome.

Results

An enlarged, homogeneously to heterogeneously attenuating and contrast‐enhancing pancreas with ill‐defined borders was identified in all dogs. CT identified more features characterizing pancreatic abnormalities compared to US. Thrombi were found in 3/10 dogs. Three dogs with heterogeneous contrast enhancement had an overall poorer outcome than those with homogenous enhancement.

Conclusions and Clinical Importance

CT angiography under sedation was used in dogs to confirm clinically suspected pancreatitis and identified clinically relevant and potentially prognostic features of pancreatitis in dogs.     

Histopathological changes in the pancreas due to decreased pancreatic blood flow in a canine tachycardia-induced cardiomyopathy model

In dogs, pancreatic acinar cell injury is thought to be caused by decreased pancreatic blood flow due to heart failure. In previous our report, it demonstrated that decreased heart function causes a significant decrease in pancreatic blood flow in heart failure dog model caused by rapid ventricular pacing (RVP). However, the types of histopathological changes remain unclear. We aimed to verify the types of histopathological changes occurring in the pancreatic tissue due to decreased heart function. After RVP for 4 weeks, atrophy of pancreatic acinar cells, characterized by a decrease in zymogen granules, was observed in all areas of the pancreas. In conclusion, the result of this study suggests that attention should be paid to ischemia/hypoperfusion injury in the pancreas.