Pancreatitis In Dogs Research Articles

Ultasonographic Findings of Pancreatitis in Dogs

Ultasonographic Findings of Pancreatitis in Dogs

Computed tomographic angiography and ultrasonography in the diagnosis and evaluation of acute pancreatitis in dogs.

BackgroundAcute pancreatitis in dogs is an under‐diagnosed disease. Current diagnostic methods are insufficient at identifying sequelae and lack prognostic capability. Computed tomographic angiography (CTA) is accurate for diagnosis and prognostication of pancreatitis in humans.ObjectivesIn comparison to ultrasound (US), CTA will (1) better diagnose more severe pancreatitis and sequelae and (2) provide assessment of patient outcome by identification of pancreatic contrast enhancement patterns.AnimalsTwenty‐six client‐owned dogs suspected to have acute pancreatitis.MethodsUS and CTA examinations performed at time of admission were compared to determine the detection of pancreatic changes and sequelae. CTA findings also were compared to outcome indicators for prognosis of dogs with acute pancreatitis. Specific canine pancreatic lipase (cPL) samples were obtained and compared with CTA findings.ResultsTen of 26 dogs had heterogeneous contrast enhancement of the pancreas. Compared to US, CTA better identified portal vein thrombosis (P = .003). Patients with heterogeneous contrast enhancement had longer hospitalization (P = .01), including hospital stays for >5 days (P = .02), had more relapses, and were more likely to have portal vein thrombosis (P = .002). Patients with heterogeneous contrast enhancement had increased spec cPL (P = .006).Conclusions and Clinical ImportanceIn comparison to US, CTA better identified dogs with more severe acute pancreatitis and those with portal vein thrombosis, factors that may predict longer hospitalization and increased risk of relapse. The presence of heterogeneous contrast enhancement and portal vein thrombosis may change therapy for patients with acute pancreatitis.

Malarone® Induced Pancreatitis and Alopecia in Dogs

Malarone® Induced Pancreatitis and Alopecia in Dogs

Evidence surrounding feeding the canine pancreatitis patient

There are many scenarios in practice where animals present with acute, chronic, and acute on chronic bouts of pancreatitis. By investigating the risk of pancreatitis in association with high fat diets in a clinical setting, dietary manipulation could be instigated to reduce the risk of pancreatitis or the risk of recurrence. Many animals are placed on low fat diets when diagnosed with pancreatitis, but there are no evidence-based fat levels suggested for these animals. Nutritional recommendations for adult dogs are a minimum of 5.5 g per 100 g dry matter of the food consumed, based on an energy requirement of 95 kcal/kg bwt0.75; there is no recommendation on the type of fats, but that the essential fatty acids are provided. A review of evidence concerning fat levels indicates that hyperlipidaemia will predispose to pancreatitis, but no defined levels have been published.

Analytical Study of Pancreatitis in Dogs

Analytical Study of Pancreatitis in Dogs

Current concepts in the diagnosis of pancreatitis in dags and cats

Pancreatitis is the most common disorder of the exocrine pancreas in both dogs and cats. Ante-mortem diagnosis of pancreatitis can be challenging and the majority of cases is believed to remain undiagnosed. Complete blood count, serum biochemistry profile and urinalysis should always be performed in dogs and cats suspected of having pancreatitis, although findings are non-specific for pancreatitis. Abdominal ultrasonography is very useful for the diagnosis of pancreatitis, although the diagnostic utility depends largely on the clinician's experience. Abdominal radiography is a useful diagnostic tool for the exclusion of other diseases that may cause similar clinical signs to those of pancreatitis. Computed tomography has not been shown to be useful for the diagnosis of canine or feline pancreatitis and thus it cannot be recommended. Histopathologic examination of the pancreas is the only method to definitively diagnose pancreatitis, but exclusion of the disease is difficult. Serum amylase and lipase activities are of no clinical value in cats and should not be used for the diagnosis of pancreatitis in this species. In dogs, these tests may still have some clinical utility as an initial approach to animals with suspected pancreatitis. Due to its low sensitivity, serum TLI concentrations are considered of limited usefulness in diagnosing pancreatitis in dogs and cats. Finally, serum PLI concentrations are currently considered to be the most sensitive and specific test for the diagnosis of canine and feline pancreatitis.

Canine pancreatitis—a challenging disease. Part 2

Canine pancreatitis poses a challenge for patients, their owners, and veterinary surgeons, not only because of the difficulty in diagnosing this disease, but also in its treatment. Treatment of canine pancreatitis generally consists of four cornerstones (intravenous fluid therapy, analgesia, nutritional support and controlling nausea), however every dog with pancreatitis presents slightly differently and each patient will need specifically tailored therapy. In human medicine, systems for measuring disease severity, monitoring disease progression and treatment options have been widely studied, but for dogs this information is much less available. This poses a challenge in getting the correct dog-specific recommendations for the treatment of pancreatitis, as many treatment recommendations are derived initially from the human field. Scoring disease severity is of practical interest not only in identifying severe cases early, but also for monitoring disease progression. The prognosis for canine pancreatitis is generally good in mild cases, which usually lead to complete resolution of clinical signs. Recurrent bouts of pancreatitis can lead to chronic pancreatitis, or worsening of the disease, with rare long-term complications possible such as diabetes mellitus or exocrine pancreatic insufficiency, bringing further challenges to patient management.

Retrospective evaluation of the impact of early enteral nutrition on clinical outcomes in dogs with pancreatitis: 34 cases (2010-2013).

To evaluate the effect of early enteral nutritional therapy on time to return to voluntary intake, maximum food consumption, incidence of gastrointestinal intolerance (GI), and total hospitalization time for dogs with acute pancreatitis. Retrospective analysis of dogs with pancreatitis at a veterinary teaching hospital between 2010 and 2013. Thirty-four client-owned dogs diagnosed with acute or acute-on-chronic pancreatitis. Medical records of dogs evaluated for inappetence, anorexia, and GI for which a diagnosis of pancreatitis was recorded were reviewed. The time to initiation of food offerings since hospitalization were recorded in addition to signalment, historical medical conditions, chief complaint, physical examination findings, diagnostic results, treatments provided, timing of food offering (within 48 h of hospitalization, early feeding group (EFG) versus delayed feeding group (DFG), diet therapy (low fat versus high fat), caloric intake (% resting energy requirement), incidence of GI (%), and length of hospitalization (LOH) (days). A Clinical Severity Index Score (CSIS) was determined for each patient. Dogs in the EFG demonstrated a decreased time to return of voluntary intake (2.1 days, EFG versus 2.7 days, DFG; P = 0.05) and time (days) to maximum intake (3, EFG versus 3.4 DFG) as compared to the DFG dogs. The DFG exhibited more GI versus EFG irrespective of CSIS grouping (60% versus 26%, P = 0.04). A CSIS ≥ 7 was associated with prolonged LOH (P = 0.004); however, time to initiation of feeding and diet selection did not impact LOH (P = 0.8). Results of the study suggested that feeding within 48 hours of hospitalization for canine pancreatitis has a positive impact on return to voluntary intake and decreases the frequency of GI in these patients, independent of CSIS. The traditional protocol of withholding food during hospitalization may not be necessary nor yield the most benefit for patient recovery; subsequently early enteral refeeding should be considered.

Canine pancreatitis — a challenging disease. Part 1

Canine pancreatitis poses a challenge for patients, their owners and veterinary surgeons. Although pathways leading to pancreatitis and its clinical signs have been extensively researched, its exact cause mostly remains unclear and is thought to be the result of multiple factors. Dogs of any age, breed or sex can develop the disease, although some breeds are over represented. Clinical signs of pancreatitis can vary from mild lethargy, anorexia, and transient vomiting to marked abdominal pain, cardiovascular shock, multi-organ failure and in severe cases death. The diagnosis of pancreatitis is supported by elevations in amylase, lipase, cPLI, SNAP cPL and Spec cPL and often followed by diagnostic imaging to confirm the diagnosis and exclude concurrent disease. Histopathology still remains the gold standard in diagnosing pancreatitis, however collection of these samples poses a challenge due to invasiveness, cost and risk of complications. Over the past years, advancements have been made with new markers, and alternative methods of available markers, to aid the diagnosis of pancreatitis. Diagnosis of pancreatitis still remains a diagnostic challenge, relying on clinical judgement as well as supportive biochemical and imaging findings.

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.

Assessment of severity and changes in C-reactive protein concentration and various biomarkers in dogs with pancreatitis.

Canine pancreatitis is a relatively common disorder, and its mortality rate remains high. However, prognostic factors for pancreatitis based on evidence are limited. Moreover, the relationship between changes in C-reactive protein (CRP) concentration—an important prognostic factor for human patients with acute pancreatitis—and the prognosis of dogs with pancreatitis has not been widely studied. Therefore, we examined prognostic factors for canine pancreatitis during the first medical examination and evaluated the usefulness of serial CRP measurements during hospitalization. Sixty-five dogs met the inclusion criteria, including 22 that were hospitalized and treated. In Study 1, a multivariate analysis revealed that three factors— decreased platelet count and a marked (greater than 1,000 µg/l) elevation of specific canine pancreatic lipase (Spec cPL) concentration at the first medical examination, as well as elevated blood urea nitrogen (BUN) and/or creatinine (CRE) level—were significantly different between the survivors and nonsurvivors. Moreover, CRP concentrations on the third and fourth days were significantly different between the two groups in Study 2. An evaluation of the decreased platelet count, remarkable elevation of Spec cPL concentration at the first medical examination, elevation of BUN and/or CRE as well as serial CRP concentration measurements may be useful for predicting the prognosis of canine pancreatitis.

New advances in the diagnosis of canine and feline liver and pancreatic disease

The diagnosis of liver and pancreatic disorders in dogs and cats present their own set of challenges. However, as new diagnostic tests are developed and the optimal ways in which to use existing tests are determined, the ability of the veterinary profession to make these diagnoses continues to improve. Histopathological assessment is considered to be the reference standard for the diagnosis of many hepatic and pancreatic diseases, but it has some inherent limitations.New classes of diagnostic tests for liver disease that are currently being studied include direct and indirect serum markers of hepatic fibrosis, such as hyaluronic acid; novel markers of hepatocellular injury, such as circulating microRNAs; and quantitative tests of hepatic microsomal function. Assays for pancreas-specific lipase have greatly improved the ability of practitioners to diagnose pancreatitis in dogs and cats. However, further research is needed to fully understand the characteristics of these assays, especially in patients with concurrent non-pancreatic disease. The more common use and refinement of CT and MRI to assess the hepatobiliary system and pancreas of dogs and cats also have huge potential to improve diagnostic capabilities.

犬の膵炎に関するアップデート ～病態から栄養管理まで～:1．病態

犬の膵炎に関するアップデート ～病態から栄養管理まで～:1．病態

Evaluation of Canine Pancreas-Specific Lipase Activity, Lipase Activity, and Trypsin-Like Immunoreactivity in an Experimental Model of Acute Kidney Injury in Dogs.

BackgroundDiagnosis of pancreatitis in dogs is complicated by extrapancreatic disorders that can alter the results of laboratory tests. Extrapancreatic disorders can also affect the diagnosis of exocrine pancreatic insufficiency (EPI). The effects of acute kidney injury (AKI) on pancreas‐specific lipase activity (Spec cPL ® Test), serum lipase activity and trypsin‐like immunoreactivity (TLI) in dogs have not been evaluated.Hypothesis/ObjectivesSerum Spec cPL, lipase activity, and TLI concentrations will increase secondary to decreased kidney function.AnimalsFive purpose‐bred dogs.MethodsExperimental prospective study. Gentamicin was used to induce AKI in 5 purpose‐bred dogs. Serum samples were collected for measurement of creatinine, Spec cPL, lipase activity and TLI over 60 days, during both induction of, and recovery from, AKI.ResultsAll dogs developed and recovered from AKI. Six of 52 (12%) serum Spec cPL concentrations were increased (2 in the equivocal zone and 4 consistent with pancreatitis) in 2 of 5 (40%) dogs. Two of 51 (4%) serum lipase activity values were increased in 2 of 5 dogs. Serum TLI was increased above the reference range in 17 of 50 (34%) samples in 3 of 5 dogs. For all biomarkers, there was no consistent correlation with increases in serum creatinine concentration.Conclusions and Clinical ImportanceDecreased renal excretion during experimental AKI did not cause consistent and correlated increases in serum Spec cPL, lipase activity, or TLI in this cohort of dogs.

Pathophysiological Effects of Pancreatic Sympathetic Denervation in Acute Necrotizing Pancreatitis in Dogs

The aim of this study was to investigate the influence of the greater splanchnic nerve (GSN) transection on the pathophysiological process of acute necrotizing pancreatitis (ANP). The dogs were divided into a sham operation (SO) group, ANP group, and ANP with bilateral GSN transection (GSNT) group. Dogs in the GSNT group underwent bilateral GSNT immediately after ANP induction. The levels of serum pancreatic amylase (AMY), calcium, high-sensitivity C-reactive protein (HCRP), tumor necrosis factor α (TNF-α), interleukin 10 (IL-10), and neutrophile granulocyte (NEU) counts were monitored dynamically, and the pathological examinations of the pancreas was performed at postoperative day 7. All the parameters among the 3 groups showed no differences before the experiment (P > 0.05). At different postoperative times, the NEU count and serum AMY, TNF-α, HCRP, and IL-10 were significantly increased; however, the serum calcium had decreased in the ANP group versus SO (P < 0.05). The postoperative serum IL-10 and calcium levels were higher, and TNF-α, HCRP, and NEU counts were lower in the GSNT group compared with those in the ANP group (P < 0.05); as for AMY, no significant difference was found between the 2 groups (P > 0.05). The pancreas pathological scoring of the GSNT group was lower versus the ANP group (P < 0.05). Greater splanchnic nerve transection can alleviate development of pathophysiological processes in ANP.

Effects of a synthetic serine protease inhibitor, camostat mesilate (FOY-305), on markers of pancreatic acinar cell damage, inflammation, and fibrosis in dogs with suspected naturally occuring chronic pancreatitis

Chronic pancreatitis is an inflammatory condition of the pancreas characterized by atrophy, fibrosis, and loss of function. Due to a lack of designated pharmaceutical agents, treatment of canine chronic pancreatitis is usually limited to supportive care. There are reports from Japan about the use of a protease inhibitor, camostat mesilate, for the treatment of chronic pancreatitis in humans, but no controlled studies about the efficacy of camostat mesilate for the treatment of chronic pancreatitis in dogs are available. Therefore, the primary goals of this study were to investigate the efficacy of camostat mesilate in dogs with suspected chronic pancreatitis as well as assess its effect on acinar cell damage by measuring serum concentrations of canine pancreas lipase immunoreactivity (cPLI). Also, the effect of the compound on systemic inflammation was quantified by measurement of serum concentrations of canine C-reactive protein and S100A12. Finally, the effect of camostat mesilate on fibrosis was assessed by measurement of serum concentrations of transforming growth factor (TGF)-β1. Thirty-one dogs with suspected chronic pancreatitis based on clinical signs and repeated measurements of an increased cPLI concentration above the cutoff value for the diagnosis of pancreatitis (≥ 400 μg/L) received a dose of 4 or 8mg/kg camostat mesilate q 8 h (12 or 24 mg/kg q 24 h) over a period of 26 ± 5 days. The evaluation of follow-up questionnaires from referring veterinarians and owners suggested improvement in quality of life in some patients. Only mild side effects were observed. Dogs given a daily camostat mesilate dose of 24 mg/kg/d orally showed a statistically significant decrease in serum cPLI concentrations between pre-treatment (median: 847 μg/L; range: 414 to 2,024 μg/L) and post-treatment (median: 520; range: 193 to 2,580 μg/L; n=19; p=0.016), indicating attenuation of acinar cell damage. Anti-inflammatory effects were comprised of a significant decrease of serum S100A12 concentrations in dogs treated with 12 mg/kg/d camostat mesilate between pre-treatment (median: 160 μg/L; range: 52 to 1327 μg/L) and post-treatment (median: 88 μg/L; range: 43 to 449 μg/L; n=11; p=0.0010). Serum cobalamin concentrations differed significantly between pre-treatment (mean: 868 ng/L; SD: ± 108ng/L) and post-treatment (mean: 695 ng/L; SD: ± 223 ng/L) concentrations in the 12 mg/kg/d group (n=12; p=0.0363) and also between pre-treatment (mean: 749 ng/L; SD: ± 229 ng/L) and post-treatment (mean: 641 ng/L; SD: ± 252 ng/L) concentrations in the 24 mg/kg/d group (n=19; p=0.045). However, no statistically significant changes in TGF-β concentrations, C-reactive protein, parameters of serum biochemistry, or complete blood counts were observed with treatment. This study would suggest a potentially beneficial role of camostat mesilate in dogs with chronic pancreatitis; however, case-control studies are needed to confirm these findings.%%%%Charakteristische Merkmale der chronischen Bauchspeicheldrusenentzundung sind Atrophie, Fibrose und…

Diagnosis of pancreatitis in dogs and cats.

Pancreatitis is the most common disorder of the exocrine pancreas in both dogs and cats. Ante-mortem diagnosis of canine and feline pancreatitis can be challenging. The clinical picture of dogs and cats with pancreatitis varies greatly (from very mild to severe or even fatal) and is characterised by non-specific findings. Complete blood count, serum biochemistry profile and urinalysis should always be performed in dogs and cats suspected of having pancreatitis, although findings are not-specific for pancreatitis. Serum amylase and lipase activities and trypsin-like immunoreactivity (TLI) concentrations have no or only limited clinical value for the diagnosis of pancreatitis in either dogs or cats. Conversely, serum pancreatic lipase immunoreactivity (PLI) concentration is currently considered to be the clinicopathological test of choice for the diagnosis of canine and feline pancreatitis. Abdominal radiography is a useful diagnostic tool for the exclusion of other diseases that may cause similar clinical signs to those of pancreatitis. Abdominal ultrasonography can be very useful for the diagnosis of pancreatitis, but this depends largely on the clinician's experience. Histopathological examination of the pancreas is considered the gold standard for the diagnosis and classification of pancreatitis, but it is not without limitations. In clinical practice, a combination of careful evaluation of the animal's history, serum PLI concentration and abdominal ultrasonography, together with pancreatic cytology or histopathology when indicated or possible, is considered to be the most practical and reliable means for an accurate diagnosis or exclusion of pancreatitis compared with other diagnostic modalities.

Pancreatitis in dogs and cats: definitions and pathophysiology.

Pancreatitis, or inflammation of the pancreas, is commonly seen in dogs and cats and presents a spectrum of disease severities from acute to chronic and mild to severe. It is usually sterile, but the causes and pathophysiology remain poorly understood. The acute end of the disease spectrum is associated with a high mortality but the potential for complete recovery of organ structure and function if the animal survives. At the other end of the spectrum, chronic pancreatitis in either species can cause refractory pain and reduce quality of life. It may also result in progressive exocrine and endocrine functional impairment. There is confusion in the veterinary literature about definitions of acute and chronic pancreatitis and there are very few studies on the pathophysiology of naturally occurring pancreatitis in dogs and cats. This article reviews histological and clinical definitions and current understanding of the pathophysiology and causes in small animals by comparison with the much more extensive literature in humans, and suggests many areas that need further study in dogs and cats.

Management of acute pancreatitis in dogs: a critical appraisal with focus on feeding and analgesia.

Knowledge about acute pancreatitis has increased recently in both the medical and veterinary fields. Despite this expansion of knowledge, there are very few studies on treatment interventions in naturally occurring disease in dogs. As a result, treatment recommendations are largely extrapolated from experimental rodent models or general critical care principles. General treatment principles involve replacing fluid losses, maintaining hydrostatic pressure, controlling nausea and providing pain relief. Specific interventions recently advocated in human medicine include the use of neurokinin-1 antagonists for analgesia and early interventional feeding. The premise for early feeding is to improve the health of the intestinal tract, as unhealthy enterocytes are thought to perpetuate systemic inflammation. The evidence for early interventional feeding is not supported by robust clinical trials to date, but in humans there is evidence that it reduces hospitalisation time and in dogs it is well tolerated. This article summarises the major areas of management of acute pancreatitis in dogs and examines the level of evidence for each recommendation.

Lifestyle and diabetes mellitus in cats and dogs

In westernised countries, obesity is the most commonly diagnosed nutritional disorder in dogs and cats, with an estimated prevalence of between 22% and 44% in investigated populations. In humans, it is well established that obesity predisposes to lifestyle-related diseases such as type 2 diabetes mellitus and atherosclerosis. Dogs and cats seem less prone to developing atherosclerosis compared with humans, while diabetes is a relatively common endocrine disease in both species. The high prevalence of obesity in pet dogs and cats is believed to be multifactorial, often relating to lifestyle and the fact that pets have moved from being working animals to becoming close family members. Influencing factors include neutering, inactivity, genetic predisposition as well as factors such as interaction with owners through feeding/treats and the owners lacking recognition of their pets being overweight. As in humans, obesity causes insulin resistance and impaired glucose metabolism in cats and dogs. In cats, this may progress into feline diabetes because long-term elevated insulin demands together with obesity-related metabolic alterations result in destruction of the beta cells – through mechanisms similar to development of human type 2 diabetes mellitus. In dogs, the pancreas seems to better cope with increasing demands for insulin production and type 2-like diabetes seldom develops. Obesity may however, still predispose for diabetes in dogs. A possible explanation could be that obese dogs are at risk of developing pancreatitis as a frequent consequence of pancreatitis in dogs is inflammation-mediated destruction of the beta cells.