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Pancreatitis in the dog and cat

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Category: Schede
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  • Disciplina: Gastroenterologia
  • Specie: Cane e Gatto

Pancreatitis is an inflammatory process that develops from the infiltration of inflammatory cells in pancreatic tissue.  It is a very common disorder of the exocrine pancreas in both the dog and cat1,2. In one study in dogs the prevalence of this disease was estimated to be about 1.7% in  9,342 samples of pancreatic tissue examined3. In another, more recent study4  only 8.2% of the pancreatic tissue samples from 208 cases did not have lesions. In the same study, nodular hyperplasia was the most frequently found lesion (84.6%). The significance of this finding is not, however, completely clear since another study found various cases of nodular hyperplasia in the absence of pancreatitis5.

 

CLASSIFICATION

A standardised classification for this disease in veterinary medicine does not exist and, therefore, the human classification is often used. Pancreatitis is divided into acute and chronic forms depending on the presence (or absence) of permanent histopathological changes such as fibrosis and acinar atrophy5,6. Other factors used to classify pancreatitis further are the presence of necrosis of peripancreatic adipose tissue and the predominant nature of the cells infiltrating the pancreatic tissue7,8 . 

From a clinical point of view both acute and chronic pancreatitis can be moderate or severe6,9. The acute form seems to more common in dogs2 while chronic pancreatitis is found more frequently in cats1. Both forms can be associated with systemic complications and local alterations such as pancreatic necrosis and effusions. However, the signs of the chronic form are usually less severe.

 

AETIOLOGY   

Only rarely is the true cause of pancreatitis identified and the condition is often considered idiopathic1. It is not yet completely clear whether chronic pancreatitis is the result of recurrent episodes of acute pancreatitis or whether it is an independent condition. It does, however, seem possible that some animals develop the chronic form after one or more episodes of acute pancreatitis10.

Some causes or risk factors for the development of pancreatitis are obesity, diets with a high-fat content, some medicines (for example, potassium bromide11,12) and infectious diseases (Toxoplasma gondii13,Amphimerus pseudofelineus14,Calicivirus15, Feline Herpevirus and feline infectious peritonitis1).

Some breeds such as miniature Schnauzer, Yorkshire Terrier, Dachshund, Labrador  and others seem to be at high risk of pancreatitis16,17. There are no studies that have analysed the histopathological features of the pancreas in detail in these breeds, but it seems that the disease is usually chronic in miniature Schnauzer. A genetically based mechanism has been hypothesised for this breed of dog18. 

Various studies in cats have associated chronic pancreatitis with inflammatory disorders of the liver and bowel19,20. The term triaditis is often used to describe the coexistence of all three disorders in the same animal. It is not clear which disorder is triggered first and what role it has in the pathogenesis of the others. This type of association does not seem to occur in dogs, although concomitant pancreatitis and inflammatory bowel disease is common in this species.

Pancreatic tumours (adenocarcinoma) and disorders causing obstruction of the biliary tree can lead to pancreatitis21.

Endocrine disorders such as hypothyroidism, hyperadrenocorticism and diabetes mellitus can cause hyperlipidaemia which, in its turn, can lead to pancreatitis22.

 

PATHOGENESIS

Various mechanisms protect the pancreas from self-digestion. First, all the proteolytic and phospholipolytic enzymes are synthesised, stored and secreted in the form of inactive zymogens.  These zymogens are stored separately and at a distance from the lysosomal enzymes to avoid their premature activation.

The zymogens have a so-called activation peptide at the end of their polypeptide chain. In normal conditions zymogens are activated in the duodenum where they are transported together with the pancreatic juices. Here they encounter enteropeptidase, produced by the duodenal cells, which converts trypsinogen into its active form of trypsin which, in its turn, cleaves the activation terminus from the zymogens, resulting in their activation.

The pancreas has some mechanisms to protect itself in the case that casual activation of the enzymes should occur. If a small amount of trypsinogen accidently becomes activated within the acinar cells of the pancreas, it hydrolyses itself, preventing the chain reaction of stimulation of zymogens. If the accidental activation of trypsin should continue, a specific inhibitor, called pancreatic secretory trypsin inhibitor, blocks the activation. Furthermore, there are a2macroglobulins in the intravascular compartment which can capture the activated zymogens and facilitate their elimination through the reticular system, while in the extravascular space there is a proteinase a1 inhibitor, although this is not sufficiently potent to be able to stop the chain reaction alone.

Once all these protective mechanisms have been overcome, the acinar cells can be damaged and numerous mediators of inflammation and free radicals may be released.  These mediators, which play a fundamental role in the progression of pancreatitis23, are released predominantly by neutrophils and macrophages. The main mediators are tumour necrosis factor-a, interleukin (IL)-1, IL-2, IL-6, IL-8, IL-10, interferon-a, interferon-b, nitric oxide and platelet activating factor23.

                                                                                                                                                                        

CLINICAL SIGNS

Animals with severe pancreatitis usually develop vomiting, abdominal pain, diarrhoea, depression and weakness.24

In very severe cases they may be systemic complications such as shock25, disseminated intravascular coagulation (DIC) and involvement of one or more organs. Animals with abdominal pain often assume a classical ‘praying’ posture (Fig. 1).  Numerous studies have shown that about 90% of human patients with pancreatitis have abdominal pain, whereas it is though that about 60% of animals with pancreatitis suffer pain24. This highlights the difficulty in interpreting the clinical signs, and in particular pain, from case to case.

Affected animals are often dehydrated because of vomiting, diarrhoea and anorexia. Ascites may occasionally be present. In patients with severe disease, complications such as bleeding, respiratory disorders, jaundice and arrhythmias may occur. The clinical signs in chronic pancreatitis may be very mild and often go unnoticed.

                                                                                                                                                                                                                                                                                                                        

DIAGNOSIS

Pancreatitis is not always an easy disorder to diagnose, particularly in a mild form with few clinical signs and clinico-pathological alterations. Blood tests, diagnostic imaging and biopsy studies with histopathological analysis are used to reach a diagnosis.

Blood tests

Amylase and lipase
For many years amylase and lipase were considered markers of pancreatic inflammation, but since they are produced by various tissues, including gastrointestinal tract tissue, kidney and liver, and because their levels can also be raised in patients with neoplasia, they are markers with a low specificity and sensitivity26.  Furthermore, since pancreatitis cannot be completely excluded in the case of normal levels of amylase and lipase, other more sensitive tests should be used. These markers have no relevance in cats and should not be used for the diagnosis of pancreatitis in this species27,28.

Trypsin-like immunoreactivity
The trypsin-like immunoreactivity (TLI) test is species-specific: it measures circulating trypsinogen and, when present, trypsin. The usefulness of this test for the diagnosis of pancreatitis is very limited in that the values of TLI can be increased for various reasons, such as gastrointestinal disorders and neoplasms19,29. The sensitivity in cats is about 28-40% while the sensitivity in dogs is around 36%1,19,30,31, severely limiting its usefulness for making a diagnosis of pancreatitis. 

Pancreatic lipase
Pancreatic lipase is synthesised in the acinar cells and enters the circulation during pancreatitis. The test for this enzyme, which is species-specific, measures the activity of only the lipase produced by the pancrease and raised levels may indicate pancreatitis. The sensitivity (>80%) and specificity of this test are higher than those of any other test available for the diagnosis of pancreatitis32,33. The test can be carried out on serum or as a snap test for a faster diagnosis.

Diagnostic imaging

Abdominal X-rays
Abdominal X-rays are neither sufficiently sensitive nor sufficiently specific to make the diagnosis of pancreatitis1,7,30. Despite this, X-rays remain a first logical approach to exclude other pathologies that can produce similar clinical signs (neoplasias, intestinal occlusion, etc.). Patients with pancreatitis often have a loss of X-ray detail in the cranial abdomen, hepatomegaly, displacement of the stomach and dilatation of the small bowel1,7,8,28,30 (Fig. 2). In a study of dogs with acute pancreatitis the sensitivity of abdominal X-rays for the diagnosis of this pathology was 28%8. Radiography is not advised as the only diagnostic technique for making or excluding a diagnosis of pancreatitis.

Abdominal ultrasound
Abdominal ultrasound in both the cat19,30 and the dog1,8 is fairly specific but has a variable sensitivity (11-70%) depending on the operator and equipment used. The possibility of diagnosing pancreatitis increases if the ultrasound study is carried out by a very expert operator19,34. Many cases of pancreatitis can be diagnosed by ultrasound, but the disorder cannot be excluded if the abdominal ultrasound appearance is within the norm. If some predefined criteria are applied during the ultrasound examination, the specificity for the diagnosis of pancreatitis increases,  although the results can sometimes be interpreted too much in favour of pancreatitis1. Ultrasound changes include the presence of free fluid in the abdomen, increased size of the pancreas, irregular parenchyma and/or hypoechogenicity and dilatation of the biliary and pancreatic ducts1,7,19,35 (Figs. 3 and 4). Ultrasonography is very useful for the diagnosis of concomitant disorders, the presence of pancreatic masses (abscesses, neoplasms), cysts (sterile, abscesses) and as an aid when performing needle aspiration biopsies of these (or  other) lesions35.

Computed tomography
Computed tomography did not give very good results in a study in cats, such that, as a diagnostic technique for pancreatitis it was inferior to abdominal ultrasound and the feline pancreatic lipase immunoreactivity (fPLI) test and is not, therefore, included among the recommended routine diagnostic investigations1,30,34. There are no studies on the use of computed tomography for the diagnosis of pancreatitis in dogs.

Histopathological studies

A histopathological examination is still the gold standard for the diagnosis of pancreatitis and for the differentiation of acute pancreatitis from chronic pancreatitis1 (Figs. 5 and 6).  However it is an invasive examination and may not reveal the disease in the case that only one part of the pancreas is evaluated. Indeed, biopsies must be taken from different parts of the pancreas and from macroscopic lesions, although these may not always be present4,36.

The diagnosis of pancreatitis is made based on the concomitant presence of appropriate clinical signs, blood and biochemical changes, an increase in pancreatic lipase, diagnostic imaging evidence and, when necessary, histopathological studies.

 

TREATMENT

Animals with pancreatitis are often dehydrated because of vomiting, diarrhoea and anorexia. The first thing to do is to stabilise these patients before starting with other diagnostic examinations.

Rehydration is fundamental for these patients: the most commonly used fluids for this purpose are Ringer’s lactate and NaCl 0.9% supplemented with KCl, given that these patients are often hypokalaemic. It is important to monitor the levels of electrolytes during the admission and correct any abnormalities (e.g. hypocalcaemia) and changes in the acid-base balance, if necessary.

In the past is was often advised that patients should not be fed for a few days to allow the pancreas “to rest”; although this may be a good strategy for patients who are vomiting a lot, there is not yet sufficient evidence to state that it is the best approach. Some studies, in both human medicine and veterinary medicine39-41,indicate that early nutritional support can have beneficial effects for the patients. These same studies demonstrated that enteral nutrition is better than parenteral nutrition for the treatment of pancreatitis, particularly in its acute form. Nutrition through a jejunal tube seems to reduce bacterial translocation from the intestine and diminish a systemic inflammatory response40,42. 

There are various strategies for providing a patient with nutrition a feeding tube, which may be jejunal (Fig. 7), gastric, oesophageal or naso-oesophageal. If the patient continues to vomit despite drug therapy, it is better not to administer food or water by mouth for 12-24 hours in order to avoid aspiration pneumonia. Subsequently a small amount of water can be given and, if the patient does not vomit, a small quantity of food. The most suitable diet in these cases is one low in fats (<10% of the dry matter); other foods should be avoided. In the case of chronic pancreatitis, it may be beneficial to limit the protein content of the diet in order that pancreatic secretion is stimulated less43.

Another fundamental part of the management of pancreatitis is the administration of analgesics, particularly in acute pancreatitis, even in the absence of evident signs of pain by the patient. Injectable opioids such as buprenorphine, methadone or morphine are very effective in reducing pain and safe-guarding the well-being of the animal during hospitalisation. Subsequently fentanyl patches or oral tramadol can be used. Care must be taken when using the patches since at least 24 hours are needed before their maximum effect is reached and if the animal is discharged from hospital the patch must be “hidden” under a dressing to avoid accidental contact by humans, in particular small children. Non-steroidal anti-inflammatory drugs must also be used prudently as they can worsen vomiting and diarrhoea because of their effects on the gastrointestinal system, or contribute to the development of acute renal failure through renal vasoconstriction and ischaemia. 

In human medicine, supplementation with pancreatic enzymes is often used because some studies seem to suggest that this can reduce sensitivity to the pain of pancreatitis37, although a meta-analysis of the effect of supplementation was not able to demonstrate the efficacy of supplements38. There are no studies on this issue in small animals.

In the case of vomiting, anti-emetics such as ranitidine, maropitant and ondansetron have been shown to give good results. The value of using metoclopramide remains doubtful given the effects of this drug on splanchnic perfusion and its use in patients with pancreatitis cannot be fully recommended.

Bacterial complications of pancreatitis are not common in small animals (unlike in human patients). Although the routine use of antibiotics has no benefit unless the patient has signs of infection (e.g. fever, neutrophilia with a left shift, toxic neutrophils), antibiotics such as amoxicillin alone or in combination with clavulanic acid, ampicillin and enrofloxacin can be used.

A lack of a2macroglobulin can lead to the death of the patient. In cases in which a deficiency of this protein is suspected, or if there are clinical signs compatible with DIC and thrombosis, the transfusion of fresh-frozen plasma is indicated. Plasma is also rich in clotting factors and albumin which can have positive effects44. In a recent study the administration of plasma was associated with a high mortality rate; however, in this study the animals in the group that received plasma were critically ill and, therefore, disadvantaged at the beginning of the study if compared to the animals that did not receive plasma45. In this same study no benefit from the administration of plasma was noted. However, as a result of other studies, the administration of plasma is strongly advised, if considered necessary44,46.

The value of the use of corticosteroids during pancreatitis is unclear. Corticosteroids can, however, be used in cases of mild pancreatitis and inflammatory bowel disease, because they are important for good control of the latter disease and do not seem to cause further problems. Budesonide, which has a topical effect, could be an option in these cases47.  In recent years there have been descriptions in the dog of a type of chronic pancreatitis, called autoimmune pancreatitis, characterized by a plasma cell infiltration48. Some authors have suggested treating patients with this form of pancreatitis with glucocorticoids which can give good results. Further studies will have to be performed before this approach can be considered as routine.

Parenteral administration of vitamin B12 (cobalamin) is advised in cats with low levels of this vitamin, since this supplementation may be of benefit to the patient49.

The administration of dopamine within 12 hours of the onset of acute pancreatitis may prevent progression of the disorder in cats50, although it is not easy to act within this short period of time in daily clinical practice.

The treatment of pancreatitis is predominantly medical although surgery may be indicated in the presence of abscesses, neoplasms, cysts or biliary duct obstruction.

 

COMPLICATIONS

Inflammation of the pancreas can extend from the exocrine pancreas to the endocrine pancreas causing progressive destruction of the islets of Langerhans and the b-cells, leading to diabetes mellitus. In one study, 28% of dogs with diabetes were found to have histological evidence of pancreatitis51.  In another study, about 51% of diabetic cats had histological evidence of chronic pancreatitis52.  However, it is still not clear whether pancreatitis can cause diabetes mellitus or not.

Exocrine pancreatic insufficiency in cats can be caused by chronic inflammation of the pancreas53,54. In dogs this pathology more frequently occurs as a result of atrophy of the acinar pancreatic cells, but also following chronic pancreatitis55.

Other complications, such as the development of abscesses, cysts and necrotic masses, may be found in patients with pancreatitis56,57. In human medicine a relationship between chronic inflammation and the development of pancreatic neoplasia has been suggested54, but in animals this has not yet been proven.

 

PROGNOSIS

The prognosis of pancreatitis is very varied. In the case of mild pancreatitis without complications, the prognosis is good.  Severe pancreatitis can, however, lead to dysfunction of various organs and, eventually, to the patient’s death. A clinical index has recent been developed for dogs with acute pancreatitis58; this index can help the veterinarian to choose a more or less intensive treatment for the patient. 

 

References

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