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Acute Necrotizing Pancreatitis in a Yellow-naped Amazon Parrot (Amazona auropalliata).

Abstract: A 25-year-old female yellow-naped Amazon parrot (Amazona auropalliata) was presented for an acute onset of lethargy, ptyalism, and regurgitation. Results of hematologic testing and plasma biochemical analysis revealed severe leukopenia and heteropenia with toxic heterophils and marked hyperamylasemia and hypoproteinemia, consistent with gastrointestinal dysfunction. Survey radiograph findings were suggestive of coelomic effusion. Results of a contrast-enhanced computed tomography (CT) scan revealed a tubular, irregularly marginated structure along the medial aspect of the duodenum, consistent with an inflamed pancreas. The bird died soon after CT imaging, and acute necrotizing pancreatitis and pancreatic coagulative necrosis were observed at necropsy. This report describes the use of a less-invasive modality such as CT to aid in the antemortem diagnosis of acute pancreatitis in a psittacine bird. Pancreatitis should be considered a differential diagnosis in birds with gastrointestinal signs and coelomic effusion visualized on radiography, and the observation of an enlarged inflamed pancreas in the absence of a defined pancreatic mass on CT.

Key words: pancreatitis, computed tomography, avian, yellow-naped Amazon parrot. Amazona auropalliata

Clinical Report

A 25-year-old female yellow-naped Amazon parrot (Amazona auropalliata) was examined at a referring veterinary facility for an acute onset of lethargy, ptyalism, and regurgitation. The parrot had no previous health issues reported by the owners and was fed a commercial pelleted diet, fresh fruits and vegetables, and cooked egg whites on a regular basis. The patient was seen shredding paper and chewing on cage toys more frequently in the 2 weeks before presentation. A blood sample collected at the referring facility was noted to be markedly lipemic, and measured analytes revealed mildly increased creatine kinase concentration (766 U/L; reference interval, 132-402 U/L). (1) Plasma lipid values were not measured at this facility.

At the referring facility, the bird was treated with lactated Ringer's solution (30 mL/kg SC q12h), enrofloxacin (15 mg/kg in SC fluid pocket q12h; Baytril 2.27%, Bayer, Shawnee Mission, KS, USA), and metronidazole (25 mg/kg PO q12h; metronidazole 500 mg, compounded in Versa Free sugarless syrup vehicle, Humeo Texarkana, TX, USA, and Ora-Plus suspending vehicle, Perrigo, Minneapolis, MN, USA) because of concern for coelomitis while pending results of diagnostic tests; calcium gluconate (100 mg/kg in SC fluid pocket q12h) because of concern for reproductive disease; and sucralfate (25 mg/kg PO 1 hour after oral medications q12h; Carafate, Aptalis Pharma US Inc., Bridgewater, NJ, USA) because of the presence of gastrointestinal signs. The patient was administered 1 dose of leuprolide acetate (800 [micro]g/ kg IM; Lupron Depot, AbbVie Inc., Chicago, IL, USA) in light of the recent reproductive behaviors and concern for reproductive disease. The next day, the bird was sedated with midazolam (1.5 mg/ kg IM) and whole-body survey radiographs were obtained. Severe decreased coelomic serosal detail was present radiographically, with effacement of most of the caudal coelomic organ margins and distension of the caudal coelomic cavity (Fig 1). Poor inflation of the lungs and air sacs was also observed and was considered a consequence of the coelomic distension. Because of the increased amount of body fat and the caudal coelomic distension in this patient, coelomic effusion was considered the primary differential diagnosis for the loss of coelomic serosal detail, followed by a caudal coelomic mass. A definitive origin for the suspected coelomic effusion was not determined radiographically. The patient subsequently was referred to the Animal Medical Center for further diagnostic imaging.

On presentation, the bird was quiet and responsive, with its eyelids partially closed and feathers fluffed. It weighed 657 g and was obese, with a body condition score of 7/9. The parrot was tachypneic with normal heart and lung sounds and the coelom was full on palpation, suggestive of fluid; however, no discrete masses were discernable. The bird was passing only urates with no fecal material, with occasional small amounts of hemorrhagic mucous. A blood sample was submitted for hematologic testing, plasma biochemical analysis, and measurement of blood lead and zinc levels, and the bird was admitted to the hospital for further supportive care and diagnostic testing. Treatments administered consisted of parenteral fluids (20 mL/kg SC q12h, lactated Ringers solution), ranitidine (1 mg/kg IM q12h), sucralfate (25 mg/kg PO q12h), metoclopramide (0.5 mg/kg IM q12h; Baxter Healthcare Corp., Deerfield, IL, USA), calcium EDTA (30 mg/kg SC once; Diamondback Drugs, Scottsdale, AZ, USA) pending results of blood lead and zinc levels, enrofloxacin (10 mg/kg SC q12h), meloxicam (0.5 mg/kg IM q12h), and gavage feedings (7 mL/kg; Exact Hand Feeding Formula, Kaytee, Chilton, WI, USA).

Results of plasma biochemical analysis revealed moderately increased activity of aspartate amino transferase (733 U/L; reference interval, 150-390 U/L), (1) severely increased activities of amylase (7113 U/L; reference interval, 187-546 U/L) (1) and creatine kinase (6505 U/L), (1) mild hypertriglyceridemia (379 mg/dL; reference interval, 10-300 mg/ dL), (2) and moderate hypoproteinemia (2.1 g/dL; reference interval, 2.6-5.9 g/fL) (3) characterized by mild hypoalbuminemia (0.7 g/dL; reference interval, 0.9-3.3 g/dL). (3) Cholesterol level was normal at 197 mg/dL (reference interval, 87-364 mg/dL) (2) and glucose level was normal at 267 mg/dL (reference interval, 246-3378 mg/dL). (1) Results of plasma protein electrophoresis and measurement of bile acid levels were within reference intervals. Abnormal results of hematologic testing revealed moderate leukopenia (4000 cells/[micro]L; reference interval, 6000-17 000 cells/[micro]L) with severe heteropenia (720 cells/[micro]L; reference interval, 3844-9052 cells/[micro]L) with a left shift (560 cells/[micro]L; reference interval, 0 cells/[micro]L), toxic change in heterophils characterized by decreased numbers of cytoplasmic granules, rounding of the granules, increased cytoplasmic basophilia, and purple coloration to some of the granules. The lymphocytes were reactive with deeper blue cytoplasm and an oval nucleus with clumped to lacy chromatin and occasionally a discernable nucleolar ring or nucleolus. These changes were consistent with severe inflammation. (1) All other test results were unremarkable, and blood lead and zinc levels were normal.

The parrot continued to regurgitate overnight. The next day, the bird was anesthetized for a whole-body computed tomography (CT) scan. Anesthesia was induced and maintained with isoflurane delivered by facemask at 2%. The bird was then intubated with a 3.5-mm uncuffed endotracheal tube, and positive-pressure ventilation was delivered intermittently during the scan. The CT images were acquired with a third-generation CT Toshiba Aquilion 64 unit (Canon Medical Systems, Tustin, CA, USA), as a volume of data (120 kVp, 100 m As), and then reconstructed in transverse, sagittal, and dorsal planes in a 1mm slice thickness, to obtain high-resolution images. Pre- and postcontrast images were acquired in soft-tissue and lung algorithms, with nonionic iodinated contrast (2.2 mL/kg; Omnipaque 300, GE Healthcare, Princeton, NJ, USA) administered by intravenous injection through the left basilic wing vein after acquisition of the initial precontrast images. Poor perfusion was noted in the peripheral veins during anesthesia, which was discontinued after the scans were complete, 30 minutes after induction. During anesthetic recovery after extubation, the patient began to regurgitate brown fluid. The oral cavity was suctioned until normal breathing resumed. An intravenous butterfly catheter was placed in the right basilic vein and a bolus of 2 mL lactated Ringer's solution was administered. The bird began to regurgitate again and subsequently went into respiratory arrest. Epinephrine (0.1 mg/kg IV) and atropine (0.2 mg/kg IV) were given to no effect. The body was submitted for a cosmetic necropsy.

The CT images revealed a moderate volume of coelomic effusion distending the coelom (Fig 2). The gastrointestinal tract was homogeneously moderately dilated with fluid, and segmental mild thickening and increased enhancement of the small intestinal wall were noted. A tubular, irregularly marginated, soft-tissue attenuating structure, moderately enhancing, was observed within the right cranial coelom, coursing along the medial aspect of the duodenum, consistent with a diffusely enlarged pancreas. The liver was heterogeneously enhancing, with ill-defined hypoattenuating areas observed predominantly within the right hepatic parenchyma on the postcontrast images. The spleen appeared mildly enlarged. The oviduct was prominent and moderately enhancing. Bilaterally, within the caudal and peripheral aspect of the lungs, increased soft-tissue attenuations were noted, effacing the normal pulmonary architecture. Finally, the amount of fat was increased within the coelomic cavity. The CT findings were consistent with acute pancreatitis, with secondary severe coelomitis, diffuse enteritis, and predominantly right-sided hepatopathy (suspected to represent hepatitis, lipidosis or a combination of both) in an obese parrot. Even though neoplasia was not completely ruled out, it was considered less likely because of the lack of defined pancreatic mass. The increased prominence and enhancement of the oviduct on the postcontrast images were considered to be secondary to inflammation.

Gross necropsy examination revealed approximately 30 mL of cloudy, yellow effusion within the coelom. This fluid was not cultured or analyzed. The intestines were diffusely, markedly dilated and reddened with multifocal petechial serosal hemorrhages, indicative of enteritis. Multiple intestinal loops were adhered to one another by pale tan, manually removable tissue (fibrin). Similar material was observed in the region of the pancreas, with yellow, red, and tan stippling, interpreted as pancreatitis, fibrinous coelomitis, mesenteric steatitis, and steatonecrosis (Fig 3). No foreign material was observed throughout the gastrointestinal tract lumen. The crop contained liquid, yellow ingesta. The hepatic parenchyma was diffusely mottled pale tan to dark brown, more prominently in the right lobe. The lungs had locally extensive regions of dark red parenchyma in the caudal regions, and sections of lung floated in formalin. Representative tissue samples from all organs were obtained, placed in 10% neutral-buffered formalin, routinely embedded in paraffin, sectioned at 5 [micro]m, and stained with hematoxylin and eosin.

Histologic evaluation of the pancreas revealed coagulation necrosis of entire lobules; severe regional necrotizing, fibrinous, heterophilic, histiocytic mesenteric steatitis; and multifocal, peripheral involvement of the viable pancreatic parenchyma (pancreatitis) (Fig 4). Occasionally, few sharply demarcated, round vacuoles (lipid) were observed within the cytoplasm of pancreatic acinar cells. The duodenum exhibited transmural, fibrinous, heterophilic and lymphoplasmacytic enteritis with multifocal necrosis. Histiocytic, heterophilic airsacculitis was present in air sacs surrounding the pancreas and throughout the coelom. Similar inflammation was observed in the capsule of the spleen. Given the type of inflammation (heterophilic, histiocytic), special stains for fungi (Gomori's methenamine silver) and acid-fast bacteria (Ziehl-Neelsen) were performed on the pancreas, mesentery, and duodenum, the results of which were negative. In the liver, lipidosis was marked with concurrent hepatitis, cholangitis, and necrosis. Granulomatous oophoritis with intralesional lipid and yolk material were present. In the lungs, heterophilic, histiocytic parabronchial pneumonia with intralesional proteinaceous and anisotropic material was observed, consistent with aspiration. Regional airsacculitis was also present. There was no histologic evidence of thrombosis in the lungs. The cause of death in this case was interpreted to be a combination of aspiration and disseminated coelomic inflammation, including necrotizing pancreatitis, mesenteric steatitis, transmural enteritis, and airsacculitis, resulting in a widespread inflammatory response and systemic sequelae.

Discussion

This clinical report is the first description of CT findings in a case of acute necrotizing pancreatitis in an adult Amazon parrot, confirmed at necropsy. Compared with the gold standard of surgical or endoscopic biopsy, CT scanning may prove to be a valuable, less-invasive modality to support the diagnosis of pancreatitis in birds. Additional antemortem diagnostic tools are needed for this disease process, as pancreatitis is often anecdotally described in birds, but comparatively few reports have been published. This case adds support to the previously described association of pancreatitis with hyperamylasemia, (4) but it also offers an additional modality to aid in diagnosis.

Similar to other animals, the avian pancreas lies between the ascending and descending loops of the duodenum and has both exocrine and endocrine functions. Most avian species have a trilobed pancreas with the third lobe, or splenic pancreas, located independent from the other two. (5) Although the intestinal wall mucosa produces some of the digestive enzymes, the pancreatic ducts also drain exocrine pancreatic enzymes into the ascending duodenal loop. In healthy birds, these digestive enzymes are secreted into the intestine as inactive precursors, preventing autodigestion of the pancreas. Acute pancreatitis is characterized by activation of these enzymes outside of the intestine, resulting in coagulation necrosis of the pancreas and surrounding tissue. (6) The presence of such large regions of coagulation necrosis in this case may reflect the severity of the pancreatitis or possible concurrent ischemic damage, although no histologic evidence of thrombosis was found. Other sources of pancreatitis may be coelomitis originating from elsewhere influencing inflammatory changes in the pancreas.

Acute necrotizing pancreatitis is rarely reported in birds and warrants further clinical investigation to determine causal or associated factors in specific cases so that ultimately treatment and prevention guidelines can be established. Quaker parrots (Myiopsitta monachus) appear particularly prone to developing acute necrotizing pancreatitis of unknown cause. (7) Interestingly, Quaker parrots seem to be especially prone to developing hyperlipidemia, although there are individuals as well as other species that develop hyperlipidemia but not pancreatic problems. (8) This case demonstrated a mild hypertriglyceridemia with normal serum cholesterol level. High-density lipoproteins, lowdensity lipoproteins, and very-low-density lipoproteins were not evaluated. Various clinical conditions that have been associated with acute pancreatitis in birds include obesity and a highfat diet, (4,9) viral infections, chlamydial infection, (10) diabetes mellitus, (11-13) toxicities, (14,15) and neoplasia. (16)

Viral infections have historically been documented as a frequent cause of pancreatitis in birds. Specific viruses associated with pancreatitis are Coronavirus, (17) herpesvirus, (18) paramyxovirus 3, (19) and flavivirus (West Nile virus). (20) A case of herpesviral-associated pancreatitis in a cockatiel (Nymphicus hollandicus) yielded inclusion bodies of the pancreatic acinar and duct cells and was also accompanied by diabetes mellitus. (18) Coronavirus in pigeons (Columba livid) is associated not only with pancreatitis but also excess mucus in the trachea, as well as pulmonary lesions. (17) Paramyxovirus has been associated with pancreatitis and also neurologic pathology in birds. (19) Some avian species infected with West Nile virus present with nonspecific clinical signs and variable reports of systemic inflammation, including pancreatitis. (20) Although this bird did not exhibit clinical neurologic deficits, the brain was not assessed because of the cosmetic necropsy performed. Viral culture and molecular diagnostic tests also were not performed.

Pancreatitis has been associated with diabetes mellitus in psittacine birds in several reports. (11-13) In a report of diabetes in a chestnut-fronted macaw (Ara severa), (12) pancreatitis was characterized as mild and considered chronic, in contrast to the clinical presentation of the parrot we describe. No evidence of diabetes, such as hyperglycemia, weight loss, polyuria, or polydipsia, was observed in the case described here. Occasional reports link heavy metal toxicosis to pancreatitis; (14,15) however, results in this bird were negative for both zinc and lead on blood measurements and gastrointestinal metallic foreign material on imaging. Obesity and hepatopathy or concurrent egg yolk coelomitis may have been contributing factors in this case.

In captivity, Amazon parrots appear particularly prone to developing obesity and secondary consequences including atherosclerosis and hepatic lipidosis. (2,21) In this parrot, fat accumulation was occasionally present within the exocrine pancreas but was not a prominent feature. The role that hypertriglyceridemia played in this case is unclear; however, consideration should be given to its relationship with the hepatic lipidosis, obesity pancreatitis, and reproductive disease observed at necropsy. In people, hypertriglyceridemia is the most common cause of acute pancreatitis after alcohol and gallstone disease. (22) Underlying pathophysiology includes hydrolysis of triglycerides by pancreatic lipase and excessive formation of free fatty acids with associated inflammation. (22) Concomitant hyperviscosity and ischemia also likely play a role. (22) In birds, the liver is stimulated during the process of egg formation to produce egg yolk precursors such as yolk-targeted, very-low-density lipoproteins, which are then reflected in circulation as a hypertriglyceridemia. (23) This bird's hypertriglyceridemia paired with oophoritis and hepatic lipidosis observed at necropsy may suggest some influence of the reproductive status in the development of pancreatitis.

The salpingitis cannot be ruled out as the initial inflammatory insult that then led to the pancreatitis; however, this is considered less likely given the relative difference in severity of inflammation between the mild inflammation observed in the reproductive tract compared with the severe necrotizing pancreatitis. Additionally, the character of the inflammation between organ systems was also different, with a granulomatous oophoritis versus heterophilic pancreatitis.

The severity of the inflammation associated with the pancreas in this parrot likely accounts for the regional air sac and intestinal inflammation. The intestinal inflammation may explain the hypoproteinemia secondary to a protein-losing enteropathy; however, the heterophilic inflammation was most severe over the intestinal serosa compared with the mucosa, indicating an extraintestinal source of inflammation. The coelomic effusion may be secondary to the pancreatitis, a primary insult that then caused pancreatitis such as hepatitis or salpingitis, protein-losing enteropathy, or a combination of all. The severe inflammatory leukogram supports the marked inflammation observed at necropsy. One study suggested amylase levels above 1500 U/L may be associated with avian pancreatitis, which is consistent with the amylase level of 7113 U/L present in this case. (4) Lipase is often measured concomitantly with amylase in small animal patients; however, this test is not useful in cats and only specific in dogs if results are orders of magnitude above the reference interval. (24,25) Although there are no reference intervals available in psittacine birds, lipase may prove useful for further supporting a diagnosis of pancreatitis. Development of a pancreas-specific lipase assay for use in birds would be a useful next step.

Treatment of acute pancreatitis is not well described in birds. In canine patients, treatment is supportive, typically aimed at replacing fluid losses, preserving hydrostatic pressure, controlling nausea, and providing pain relief. (26) Although this patient was started on appropriate supportive treatments, hypotension and aspiration compounded by general anesthesia likely led to the bird's death.

Histopathology is considered the test of choice for the diagnosis of pancreatitis. Historically, antemortem diagnosis of pancreatitis in birds has only been achieved by endoscopy or exploratory laparotomy. (4) Patient history can provide useful supporting information during assessment of suspected cases of avian pancreatitis. In this case, visceral coelomic pain may have contributed to the abnormal behaviors observed in this parrot, specifically chewing of cage items. Body condition score and high-fat diet are possible predisposing factors for pancreatitis in birds; however, more data are needed to add to existing reports. (4,9) This case is of particular importance to highlight the potential use of less-invasive modalities such as CT to aid in antemortem diagnosis of acute pancreatitis. In a healthy bird, the pancreas is normally not visualized on CT images. (27) Therefore, acute pancreatitis should be considered as a differential diagnosis in a psittacine bird with gastrointestinal signs, decreased coelomic serosal detail radiographically, and a tubular soft-tissue enhancing lesion observed along the duodenum on CT images.

Kyle A. Donnelly, DVM, MPH, Alexandre Le Roux, DVM, MS, Dipl ECVDI, Dipl ACVR, Taryn A. Donovan, DVM, Dipl ACVP, Jessica Grodio, DVM, PhD, and Katherine Quesenberry, DVM, MPH, Dipl ABVP (Avian)

From Avian and Exotic Pet Service (Donnelly, Quesenberry), Diagnostic Imaging Service (Le Roux), and Anatomic Pathology Service (Donovan), The Animal Medical Center, 510 E 62nd St, New York, NY 10065, USA; and South Wilton Veterinary Group. 51 Danbury Rd. Wilton, CT 06897, USA (Grodio). Present address: University of Florida College of Veterinary Medicine. Zoological Medicine Service, PO Box 100126, 2015 SW 16th Ave. Gainesville FL 32610, USA (Donnelly); The Center for Avian and Exotic Medicine. 562 Columbus Ave. New York. NY 10024. USA (Grodio).

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(12.) Pilny A, Luong R. Diabetes mellitus in a chestnut-fronted macaw (Ara severa). J Avian Med Surg. 2005; 19(4):297-302.

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(18.) Phalen DN, Falcon M, Tomaszewski EK. Endocrine pancreatic insufficiency secondary to chronic herpesvirus pancreatitis in a cockatiel (Nymphicus hollandicus). J Avian Med Surg. 2007;21(2): 140 145.

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Caption: Figure 1. (A) Right lateral and (B) ventrodorsal whole-body radiographs of an Amazon parrot that presented with acute onset of lethargy, ptyalism, and regurgitation. Coelomic serosal detail is severely decreased, with effacement of most of the caudal coelomic organ margins and distension of the caudal coelomic cavity (black asterisk). An increased amount of body fat is also noted radiographically (white arrowheads). Coelomic effusion is considered most likely based on these radiographic findings. Note the decreased pulmonary/air sac inflation, likely secondary to caudal coelomic distension (white # signs).

Caption: Figure 2. Select computed tomography (CT) images of the Amazon parrot described in Figure 1, acquired with a third CT generation Toshiba Aquilion 64 unit (Canon Medical Systems, Tustin, CA, USA) as a volume (120 kVp, 100 mAs), and then reconstructed in transverse, sagittal, and dorsal planes, in a 1-mm slice thickness, to obtain high-resolution images. (A) Dorsal multiplanar reconstruction (MPR) in a lung algorithm, precontrast. Bilateral soft-tissue attenuations are visible within the caudal lungs (black arrows), considered to represent either pneumonia or pulmonary thromboemboli. On images (B) to (E) (multiplanar reconstruction images in a soft-tissue algorithm, postcontrast), moderate coelomic effusion is present (white asterisk), with a tubular, irregularly marginated, soft-tissue attenuating structure, moderately enhancing, observed within the right cranial coelom, (D) coursing along the medial aspect of the duodenum, and consistent with an enlarged inflamed pancreas (white arrows). The gastrointestinal tract is homogeneously moderately dilated with fluid, and segmentally, mild thickening and abnormal enhancement of the small intestinal wall is noted on these images, consistent with enteritis. (B, D, E) Additionally, the liver is heterogeneously enhancing, as visualized on these images, with ill-defined hypoattenuating areas observed within the right hepatic parenchyma (white arrowheads), and suspected to represent hepatitis, lipidosis, or a combination of both.The image inset associated with each subfigure represents the plan of the displayed CT images. (A-D) The right of the patient is on the left on images.

Caption: Figure 3. The intestines and mesentery at necropsy of the Amazon parrot described in Figure 1. The intestines are diffusely, markedly dilated and reddened with multifocal petechial serosal hemorrhages. Multiple intestinal loops are adhered to one another by pale tan, manually removable material (fibrin). Similar material is observed in the region of the pancreas (arrow), with yellow, red, and tan stippling (asterisk), consistent with pancreatitis, coelomitis, fibrinous mesenteric steatitis, and steatonecrosis (bar = 1 cm).

Caption: Figure 4. The pancreas and mesentery of the Amazon parrot described in Figure 1. Coagulation necrosis of an entire pancreatic lobule (asterisk) with severe regional necrotizing, fibrinous, heterophilic, histiocytic mesenteric steatitis (arrows). (Hematoxylin and eosin, X40 magnification, bar = 200 [micro]m.) Inset: High-magnification view of heterophilic, histiocytic, necrotizing mesenteric steatitis (arrow). (Hematoxylin and eosin. X500 magnification, bar = 20 [micro]m.)
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Title Annotation:Clinical Report
Author:Donnelly, Kyle A.; Roux, Alexandre Le; Donovan, Taryn A.; Grodio, Jessica; Quesenberry, Katherine
Publication:Journal of Avian Medicine and Surgery
Date:Sep 1, 2018
Words:4342
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