Pancreatic Torsion Resulting in Acute Pancreatic Necrosis in a Young Dog.

We report a case of 7 mo old French bulldog who was referred to North Carolina State University Small Animal Emergency and Triage Services because of acute abdomen, regurgitation, lethargy, and fever. The patient had a history of pulmonic stenosis, which was corrected by balloon valvuloplasty 3 wk before presenting for the current complaint. The patient had nonspecific changes noted on blood work at his referring veterinarian. An abdominal ultrasound examination showed pathological changes that were supportive of a left-limb pancreatic torsion that was confirmed postmortem.

Clinical characteristics and outcomes of pancreatic fungal infection in patients with necrotizing pancreatitis.

Pancreatic fungal infection (PFI) in patients with necrotizing pancreatitis can lead to significant morbidity and mortality. The incidence of PFI has increased during the past decade. Our study aimed to provide contemporary observations on the clinical characteristics and outcomes of PFI in comparison to pancreatic bacterial infection and necrotizing pancreatitis without infection. We conducted a retrospective study of patients with necrotizing pancreatitis (acute necrotic collection or walled-off necrosis), who underwent pancreatic intervention (necrosectomy and/or drainage) and had tissue/fluid culture between 2005 and 2021. We excluded patients with pancreatic procedures prior to hospitalization. Multivariable logistic and Cox regression models were fitted for in-hospital and 1-year survival outcomes. A total of 225 patients with necrotizing pancreatitis were included. Pancreatic fluid and/or tissue was obtained from endoscopic necrosectomy and/or drainage (76.0%), CT-guided percutaneous aspiration (20.9%), or surgical necrosectomy (3.1%). Nearly half of the patients had PFI with or without concomitant bacterial infection (48.0%), while the remaining patients had either bacterial infection alone (31.1%) or no infection (20.9%). In multivariable analysis to assess the risk of PFI or bacterial infection alone, only previous pancreatitis was associated with an increased odds of PFI vs. no infection (OR 4.07, 95% CI 1.13-14.69, p = .032). Multivariable regression analyses revealed no significant differences in in-hospital outcomes or one-year survival between the 3 groups. Pancreatic fungal infection occurred in nearly half of necrotizing pancreatitis. Contrary to many of the previous reports, there was no significant difference in important clinical outcomes between the PFI group and each of the other two groups.

We examined 225 patients with necrotizing pancreatitis who had tissue/fluid culture available and found that nearly half of the patients had pancreatic fungal infection. Interestingly, there was no difference in clinical outcomes between the fungal infection group and non-fungal infection groups.

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.

Comparative pathogenicity of two subtypes (hepatitis-type and pancreatitis-type) of duck hepatitis A virus type 1 in experimentally infected Muscovy ducklings.

Duck hepatitis A virus type 1 (DHAV-1) causes acute hepatitis with high morbidity and mortality in ducklings of the genera Cairina and Anas and is characterized by ecchymotic haemorrhage and necrosis of the liver surface. Since September 2011, a new subtype of DHAV-1 (named pancreatitis-type DHAV-1) has been isolated. This new subtype is characterized by yellowish or haemorrhagic pancreatitis, but with no significant pathological changes in the liver. To further investigate the difference in pathogenicity between hepatitis-type DHAV-1 and pancreatitis-type DHAV-1, we infected Muscovy ducklings with a hepatitis-type DHAV-1 strain, FZ86, or a pancreatitis-type DHAV-1 strain, MPZJ1206, and then compared the resulting gross lesions, histopathological changes, viral distribution and cellular apoptosis in the liver and pancreas of Muscovy ducklings. The results suggested that FZ86 induced a more efficient viral propagation in the liver than MPZJ1206, and the gross and histopathological lesions were also limited to the liver. However, MPZJ1206 induced more effective viral replication in the pancreas than FZ86. The MPZJ1206-infected Muscovy ducklings showed an obviously yellowed and haemorrhagic pancreas, but with no significant pathological changes in the liver. Furthermore, FZ86 induced notable hepatocyte apoptosis and increased the expression of caspase-3 in the liver, whereas MPZJ1206 caused apoptosis in a large number of acinar epithelial cells and elevated the expression of caspase-3 in the pancreas. Taken together, these results demonstrated that pancreatitis-type DHAV-1 has many new pathogenic features which distinguish it from the hepatitis-type DHAV-1. RESEARCH HIGHLIGHTS Pancreatitis-type DHAV-1 (MPZJ1206) was characterized by pancreatic haemorrhage and yellow discolouration, but with no obvious haemorrhage and necrosis in the liver. Pancreatitis-type DHAV-1 (MPZJ1206) exhibits many new pathogenic features which distinguish it from the hepatitis-type DHAV-1 (FZ86).

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

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.

Left subclavian artery dissection associated with connective tissue abnormalities resembling Marfan-like syndrome in an English bulldog.

The unexpected demise of a 12-year-old male neutered English bulldog solicited a gross examination, which revealed a blood-filled space occurring in the proximal left subclavian artery (LSA). It originated about 1 cm from the branching point of the vessel and progressively dilated for 3 cm distal to this origin. Histopathological investigation showed that the tunica media of the LSA was more than 50% split, with the blood-filled space dissecting through the arterial wall. In the tunica media of the LSA, severe multifocal fragmentation and/or loss of the elastic fibers was observed. The retained disorganized elastic fibers were separated and disoriented due to accumulations of acid mucopolysaccharide. Marked, diffuse medial, and adventitial fibrous tissue deposition was also identified. The cause of death was attributed to acute hemorrhagic and necrotizing pancreatitis with pulmonary edema, suggesting that LSA dissection was an incidental finding. Subclavian artery dissection is extremely rare in humans, where the involvement of the LSA in cases of aortic dissection both with or without Marfan syndrome has been reported. Aortic and pulmonary artery dissection in bovines and aortic aneurysm and dissection in dogs have been reported to be associated with Marfan and Marfan-like syndromes, respectively. Histopathological findings suggestive of underlying connective tissue abnormalities resembling Marfan-like syndrome (i.e., the appearance of the elastic tissue and the degenerative changes of the tunica media) were detected in the first case of LSA dissection in dogs and veterinary medicine, herein described.

Intermediate-grade mammary gland adenocarcinoma in an 18-year-old female black leopard (Panthera pardus) with acute pancreatic necrosis and chronic interstitial nephropathy.

An 18-year-old female black leopard (Panthera pardus) showed renal failure, leukocytosis and presence of subcutaneous masses in the lower abdominal region and right shoulder; she eventually died. Histopathological observations included a mammary gland carcinoma with comedo, solid and tubulopapillary patterns in subcutaneous tissue, and highly proliferated tumor cells in systemic organs. The tumor cells were positive for cytokeratin AE1/AE3. The mammary gland tumor was diagnosed as intermediate-grade adenocarcinoma, based on a previously reported histological grading system of feline mammary carcinomas. Chronic interstitial nephritis was estimated to have been ongoing for 5 years, whilst acute necrotic pancreatitis in relation to tumor metastasis could have been the cause of death.

Lung Inflammation Associated With Clinical Acute Necrotizing Pancreatitis in Dogs.

Although dogs with acute necrotizing pancreatitis (ANP) can develop respiratory complications, there are no data describing lung injury in clinical cases of ANP in dogs. Therefore, we conducted a study to characterize lung injury and determine if pulmonary intravascular macrophages (PIMs) are induced in dogs with ANP ( n = 21) compared with control dogs ( n = 6). Two pathologists independently graded histologic sections of pancreas from clinical cases to characterize the severity of ANP (total scores of 3-10) compared with controls showing histologically normal pancreas (total scores of 0). Based on histological grading, lungs from dogs with ANP showed inflammation (median score, 1.5; range, 0-3), but the scores did not differ statistically from the control lungs (median score, 0.5; range, 0-2). A grid intersects-counting method showed an increase in the numbers of MAC387-positive alveolar septal mononuclear phagocyte profiles in lungs of dogs with ANP (ratio median, 0.0243; range, 0.0093-0.0734, with 2 outliers at 0.1523 and 0.1978) compared with controls (ratio median, 0.0019; range, 0.0017-0.0031; P < .0001). Only dogs with ANP showed labeling for von Willebrand factor in alveolar septal capillary endothelial cells, septal inflammatory cells, and alveolar macrophages. Toll-like receptor 4 and interleukin 6 were variably expressed in alveolar macrophages and septal inflammatory cells in lungs from both ANP and control dogs. Inducible nitric oxide synthase was detected in alveolar macrophages of dogs with ANP only. These data show that dogs with ANP have lung inflammation, including the recruitment of PIMs and expression of inflammatory mediators.

Haemolytic anaemia and acute pancreatitis associated with zinc toxicosis in a dog.

We describe a case of zinc toxicity in a 14-month-old, female, neutered, Cavalier King Charles spaniel with a 48-hour history of haematochezia, icterus and collapse. Regenerative anaemia with a packed-cell volume of 7 per cent was seen. Prior to referral, radiography had revealed a gastric, metallic foreign body which was removed at exploratory laparotomy. On presentation, the dog was comatose, hypothermic and bradycardic - resuscitation was performed successfully, but the dog then displayed marked abdominal pain. The dog died 12 hours after presentation. At postmortem examination, the animal showed severe icterus. Both kidneys were diffusely dark red; the pancreas was diffusely pale and nodular. Histopathological examination revealed evidence of intravascular haemolysis with blood vessel lumens containing haemoglobin. The renal tubules also contained large amounts of intraluminal haemoglobin with haemoglobin crystals scattered throughout the cortex and medulla. The pancreas exhibited multifocal coagulative necrosis, surrounded by a neutrophil-dominated inflammatory infiltrate. Zinc levels were markedly increased above the normal reference range in both liver and kidney. This report describes the clinical and pathological findings of a case of acute zinc toxicity in a dog following ingestion of a metallic object which resulted in marked haemolytic anaemia and acute pancreatitis.

Pathologic and immunohistochemical studies of Newcastle disease (ND) in broiler chickens vaccinated with ND: severe nonpurulent encephalitis and necrotizing pancreatitis.

Twenty-five 22- to 46-day-old broilers with Newcastle disease (ND) were investigated pathologically and immunohistochemically in order to evaluate the mechanism of ND outbreak in vaccinated broilers. The broilers were vaccinated with ND live vaccine via drinking water. Clinical signs were neurologic and respiratory in nature. Macroscopically, bursal atrophy, white spots on the pancreas, and discoloration and enlargement of kidneys and spleen were observed in the broilers. Histologically, perivascular cuffing, neuronal degeneration and necrosis, and glial proliferation were present in the cerebrum, cerebellum, and medulla oblongata. There was extensive rarefaction and malacia in the parenchyma of severely affected brains. There were extensive degeneration, necrosis, and depletion of acinar cells in the pancreas. There was proliferation of macrophages in the lungs with congestion, tubulointerstitial nephritis, hepatocytic necrosis with thrombi in the sinusoids, and lymphocytic depletion in the cloacal bursa. Immunohistochemically, ND virus antigens were detected in the lesions. ND virus isolated from the present cases did not cause encephalitis or pancreatitis in specific-pathogen-free chickens, but it induced mortality with hepatocytic sinusoidal thrombi, splenic necrosis, lymphoid necrosis and depletion, and conjunctival hemorrhage. Severe nonpurulent encephalitis with extensive rarefaction and malacia, and necrotizing pancreatitis in the present case may suggest a close possibly causal relation with vaccination.

Effects of curcumin on tumour necrosis factor-alpha and interleukin-6 in the late phase of experimental acute pancreatitis.

Summary Inflammatory cytokines have been demonstrated to play an important role in the induction and severity of acute pancreatitis (AP) in the recent studies. The aim of this study was to investigate the effects of curcumin on inflammatory cytokines, such as tumour necrosis factor (TNF)-alpha and interleukin (IL)-6 in the late phase of AP. The study was conducted on 40 male Wistar Albino rats. The animals were divided randomly into four equal groups. AP was induced by the infusion of 3% sodium taurocholate into the biliopancreatic duct (in groups I and II). Starting on day 20 prior to the induction of AP, rats in group I received daily dose of 100 mg/kg of curcumin, dissolved in 9% ethanol via an intragastric tube. The same procedure was repeated for 6 days following the onset of AP. Group III was infused only on saline solution. Group IV (curcumin control group) received 9% ethanol via an intragastric tube, during the experimental period (totally 26 days). All the animals were sacrificed on day 6 after the collection of blood samples and serum TNF-alpha and IL-6 levels were determined. Tissue samples were taken from pancreas, mesenteric lymph nodes, liver, lungs, spleen and the kidneys for histopathological evaluation. Serum TNF-alpha and IL-6 levels in the group, which received curcumin (group I), were determined to be significantly lower than those of the untreated group (group II) (P<0.05). No statistically significant difference was detected in terms of total histopathological scores in the treatment group versus untreated group. Curcumin has been shown to markedly reduce serum TNF-alpha and IL-6 levels in the late phase of AP, but failed in the prevention of tissue injury.

Acute necrotising pancreatitis following grain overload in a donkey.

A donkey developed abdominal discomfort and distension together with cardiovascular collapse and gastric reflux 24 to 36 hours after ingesting a large amount of poultry feed. Rectal findings prompted a laparotomy that identified extensive gastric dilation, an empty, atonic small intestine, dry colonic content and an easily corrected caecal displacement. These findings were not consistent with the severity of the signs, which were attributed to endotoxaemia. The donkey was euthanased during recovery. Necropsy revealed acute necrotising pancreatitis with massive gastric dilation and right dorsal colon impaction. The clinicopathological features of acute equine pancreatitis associated with grain overload are discussed.

Clinical differentiation of acute necrotizing from chronic nonsuppurative pancreatitis in cats: 63 cases (1996-2001).

OBJECTIVE: To characterize clinical, clinicopathologic, radiographic, and ultrasonographic findings in cats with histologically confirmed acute necrotizing pancreatitis (ANP) or chronic nonsuppurative pancreatitis (CP) and identify features that may be useful in the antemortem differentiation of these disorders. DESIGN: Retrospective study. ANIMALS: 63 cats with histologically confirmed ANP (n = 30) or CP (33). PROCEDURE: Medical records were reviewed for signalment, clinical signs, concurrent diseases, clinicopathologic findings, and results of radiography and ultrasonography. RESULTS: Cats in both groups had similar nonspecific clinical signs, physical examination findings, and radiographic and ultrasonographic abnormalities. Abdominal ultrasonographic abnormalities, including hypoechoic pancreas, hyperechoic mesentery, and abdominal effusion, were found in cats in both groups and, therefore, were not specific for ANP. Cats with CP were significantly more likely to have concurrent diseases than were cats with ANP (100 and 83%, respectively). Clinicopathologic abnormalities were similar between groups; however, serum alanine aminotransferase and alkaline phosphatase activities were significantly higher in cats with CP. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that ANP and CP in cats cannot be distinguished from each other solely on the basis of history, physical examination findings, results of clinicopathologic testing, radiographic abnormalities, or ultrasonographic abnormalities.

Blood-gas and acid-base profile in dogs with severe pancreatitis.

A number of systemic disorders develop in the clinical course of acute pancreatitis. Among these important are the respiratory disorders occurring in 35-55% of the patients. They develop in the first hours after onset of pancreatitis and are the cause of death in 60% of the severe forms of acute pancreatitis. We studied the changes in the arterial blood oxygen status and acid-base status in experimentally induced severe acute pancreatitis in dogs. The animals were divided into two groups--one receiving sandostatin treatment and the other without treatment. Quickly progressing acute arterial hypoxemia was observed in the dogs with severe acute pancreatitis. Hypoxemia development was delayed by administration of sandostatin.

Ultrasonographic imaging of experimentally induced pancreatitis in cattle.

This study was conducted to determine the ultrasonographic patterns of pancreatitis evoked in cattle, with reference to laboratory and pathological findings. Using ultrasonographic guidance, acute necrotizing pancreatitis was induced in six cows by injecting chloroform into the pancreatic tissue. Ultrasonographic examination was then performed once daily for nine days. Pancreatic lesions were visible 24h after induction of pancreatitis, as represented by a uniform increase in echogenicity and by intralobular and subcapsular fluid accumulation. As the experiment progressed, patchy hypoechogenic foci appeared within the gland parenchyma. Amylase and lipase activities showed rapid increases. Post mortem examination revealed gross and microscopic necrotic and haemorrhagic lesions in the body and right lobe of the pancreas, accompanied by oedema and fibrosis. Ultrasonography was found to be extremely useful for the detection and characterization of experimentally induced pancreatitis and to monitor its progression in the cow. These findings are of potential value as a reference for the diagnostic workup of bovine pancreatitis, and ultrasonography is seen as a promising non-invasive technique for the diagnosis of suspected pancreatitis in cattle.

Pancreatic concentrations of cefepime in experimental necrotizing pancreatitis.

To evaluate the penetration of cefepime in the inflamed pancreas, three doses of 50 mg/kg were administered intramuscularly at 8-h intervals after induction of acute necrotizing pancreatitis using intraperitoneal injection of DL-ethionine in 35 rabbits and in 33 controls. Animals were sacrificed and concentrations of cefepime were determined by a microbiological assay. Cefepime reached its peak concentrations 60 min after the last drug dose when mean values of 46.05 microg/ml, 22.34 microg/g and 34.74 microg/ml were found in serum, pancreas and bile, respectively, in rabbits with acute necrotizing pancreatitis and 45.19 microg/ml, 12.68 microg/g and 20.77 microg/ml respectively in controls. Tissue/serum ratios of cefepime were 0.48, 0.23, 0.15 and 0.09 at 60, 90, 120 and 180 min, respectively, after the last dose of cefepime in rabbits with acute necrotizing pancreatitis and 0.28, 0.18, 0.16 and 0.16, respectively at 60, 90, 120 and 180 min in controls. It is concluded that the administration of cefepime in rabbits with acute necrotizing pancreatitis resulted in pancreatic tissue levels well above the MIC90s of the common pathogens involved in pancreatic superinfection, so that its administration might be proposed for the therapy of superinfection following acute necrotizing pancreatitis in humans.

Zinc-associated acute pancreatitis in a dog.

Zinc-induced haemolytic anaemia is a common phenomenon in dogs in the USA following the ingestion of pennies minted after 1982. A case of acute pancreatitis secondary to zinc toxicosis in a dog is described. Acute pancreatitis has been reported in humans, following the ingestion of liquid zinc chloride, but zinc-associated pancreatitis has not been reported previously in the dog. The mechanism of toxicity is unknown, although the pathophysiology may relate to the role of the pancreas in zinc excretion. Acute pancreatitis as a sequela to zinc toxicosis in the dog represents a complication that may prolong hospitalisation and worsen the prognosis.

Combined use of ultrasonography and contrast enhanced computed tomography to evaluate acute necrotizing pancreatitis in two dogs.

The imaging findings in two miniature schnauzers with acute necrotizing pancreatitis are described. Both dogs were treated previously for diabetes mellitus and hyperlipidemia. Vomiting, anorexia, and lethargy were observed in both dogs at presentation. Laboratory evaluations supportive of pancreatitis included left shift, abnormally high serum amylase and lipase activities, hypocalcemia, and abnormally high serum activities of liver enzymes. Sonographically, both dogs had diffusely enlarged hypoechoic pancreatic tissue with anechoic foci compatible with necrosis, abscessation, phlegmon, and pseudocysts formation. Contrast-enhanced computed tomography (CT) findings in both dogs were compatible with pancreatic necrosis. Dog 1 was managed medically for 11 days. Follow-up CT scan in this dog disclosed decreased pancreatic size and increased contrast enhancement compatible with partial resolution of pancreatitis.

Acute pancreatitis: a newly recognised potential complication of canine babesiosis.

This retrospective study describes 4 cases of canine babesiosis with histologically confirmed acute pancreatitis. In addition, 16 dogs with babesiosis are reported with serum amylase (>3500 U/l) and/or lipase (>650 U/l) activity elevations of a magnitude that would support a diagnosis of probable acute pancreatitis, although extra-pancreatic sources of the enzymes could not be excluded in these cases. Median time of pancreatitis diagnosis was 2.5 days post-admission, with primarily young (median age 3 years), sexually intact dogs affected. The development of pancreatitis was unrelated to the degree of anaemia at time of admission. In addition to pancreatitis, 80% of cases suffered from other babesial complications, namely icterus (13), acute respiratory distress syndrome (6), immune-mediated haemolytic anaemia (6), renal failure (3), haemoconcentration (2) and cerebral syndrome (2). Acute respiratory distress syndrome, renal failure and cerebral syndrome were associated with a poor prognosis, with 4 of the 5 dogs included in the overall 26% mortality rate having at least 1 of these complications. Haemolytic anaemia with ischaemia-reperfusion injury to the pancreas is proposed as a possible primary pathophysiological mechanism in babesial pancreatitis. Hypotensive shock, immune-mediated haemolytic anaemia, haemoconcentration and possibly altered lipid metabolism in babesiosis may also be involved. The previously postulated pro-inflammatory cytokine milieu of complicated babesiosis may underlie the progression, if not the primary initiation, of pancreatic pathology. Acute pancreatitis may represent the previously reported 'gut' form of babesiosis.