Feline pancreatitis (Proceedings)
Feline pancreatitis is an often thought of diagnosis in the sick cat. Cats suspected of pancreatitis commonly present with non-specific signs such as lethargy, anorexia, and dehydration. Examination findings also tend to be non-specific. Diagnosing feline pancreatitis is not as straight forward compared to diagnosing canine pancreatitis. Frequently, the feline patient with suspected pancreatitis has concurrent disease, making the diagnosis of pancreatitis more difficult. Most common diagnostic modalities are not as sensitive for feline pancreatitis and/or need to be sent to an outside laboratory, delaying definitive diagnosis. Although supportive therapy for feline patients with acute pancreatitis is similar to those for canine patients, there are some therapeutic recommendations that differ. The goals of this lecture are to help the veterinarian differentiate pancreatitis from the other disease processes, both concurrent and those with similar presentations, and then determine what traditional and ancillary therapies are warranted in treating the feline patient with acute pancreatitis.
Pathophysiology of Acute Pancreatitis
Many different inciting causes have been postulated to cause feline acute pancreatitis. Several infectious agents have been shown to cause feline pancreatitis; feline parvovirus, Toxoplasma gondii, feline herpesvirus I, Eurytrema procyonis (a fluke), feline infectious peritonitis (FIP), and, rarely, Amphimerus pseudofelineus have been implicated. Concurrent metabolic/inflammatory diseases such as diabetes mellitus, inflammatory bowel disease, cholangiohepatitis, and hepatic lipidosis have been noted to be risk factors for developing pancreatitis, although a cause and effect relationship has not been established. Scientific support for the ingestion of a high fat meal or concurrent use of Glucocorticoids as causative agents of feline pancreatitis is lacking. Blunt and penetrating trauma to the abdomen, and the pancreas specifically, can lead to severe acute pancreatitis. Hypoperfusion of the pancreas during anesthesia or shock can also lead to the development of acute pancreatitis. Despite this long list of potential causes, more than 90% of all cases of feline pancreatitis are classified as idiopathic.Irrespective of the initiating cause, pancreatitis is generally believed to occur when digestive enzymes are activated prematurely within the pancreas. In the normal pancreas, safeguards are present to ensure that harmful pancreatic enzymes are not activated until they reach the intestinal lumen. Enzymes are stored in zymogen granules within the acinar cell in the presence of pancreatic secretory trypsin inhibition and are released at the apical surface directly into the duct system. They are only activated in the intestine, by trypsin, following the cleavage of trypsinogen by enterokinase. In clinical pancreatitis, it is thought that inappropriate premature activation of trypsin from trypsinogen in the acinar cells initiates a cascade of early activation of zymogens, especially pro-elastase and pro-phospholipase, leading to auto-digestion of the pancreas. Often pancreatic inflammation is a self-limiting process, but in some animals reduced pancreatic blood flow and leukocyte and platelet migration into the inflamed pancreas may cause progression to pancreatic necrosis. Secondary infection may arise by bacterial translocation from the intestine. Release of active pancreatic enzymes and inflammatory mediators from the inflamed pancreas amplifies the severity of pancreatic inflammation, and adversely affects the function of many organs (systemic inflammatory response), and cause derangement in fluid, electrolyte and acid-base balance. It is the development of multi-systemic abnormalities that separates mild from severe, potentially fatal pancreatitis.
Diagnosis of Acute Pancreatitis
Pancreatitis tends to occur in any age, neutered cats with no gender preference. Siamese cats are over-represented. In contrast to people and dogs, obesity has not been reported to be a risk factor for pancreatitis in cats. Clinical signs of pancreatitis in cats differ markedly from that in the dog. Cats are far less inclined to have vomiting and diarrhea as presenting complaints. Indeed the most commonly reported clinical signs in the cat are lethargy and anorexia. About 64% of cases are jaundiced. Often cases have only a vague history of weight loss and behavioral change and few abnormalities are consistently detected upon examination, with dehydration and changes in body temperature most commonly reported. Abdominal discomfort, an abdominal mass, respiratory difficulty, and ataxia are inconsistently reported.
Routine laboratory testing, although essential for evaluation of other organ systems, often provides little assistance in the diagnosis of pancreatitis. Serum amylase and lipase activities have no clinical value for the diagnosis of feline pancreatitis. Radiographic changes seen in some feline patients with pancreatitis include a decreased contrast in the cranial abdomen and displacement of abdominal organs. However, these changes are rather subjective and abdominal radiography is non-specific for feline pancreatitis.
Abdominal ultrasound was, and remains, a standard test for diagnosing acute pancreatitis. The sonographic features of feline pancreatitis include hypoechogenicity of the pancreatic parenchyma, hyperechoic peri-pancreatic mesentery, pancreatic enlargement, peritoneal effusion, pancreatic mass and dilation of the pancreatic duct. It has been established that the appearance of the pancreatic duct changes with age in healthy cats. Pancreatic pseudocysts and abscesses are occasionally found by ultrasonography, and should be aspirated for cytology and aerobic culture. However, ultrasonography is not perfect: it is very operator dependent, and false positive and false negative results are possible, even in the hands of an experienced operator. Ultrasonography has been reported to have sensitivity in diagnosing feline pancreatitis of 25-80% with better results noted with more severe pancreatic inflammation. Mild cases of feline pancreatitis may appear normal on ultrasound examination.
The presence of other disease processes is frequent and emphasizes the utility of abdominal ultrasound in patients suspected pancreatitis. Hepatic lipidosis is reported in 38% of cats with acute pancreatitis, and aspiration of the liver via ultrasound guidance is warranted if suspicion is present. Another study found that 14% of cats with lymphocytic portal hepatitis and 39% of cats with cholangiohepatitis had IBD and mild pancreatitis. Many of these cases require biopsy of all three organs for definitive diagnosis as they frequently have negative, non-specific or equivocal ultrasonographic findings.
Trypsinogen and trypsin are pancreas-specific in origin and leakage into the vascular space of both is noted with pancreatitis. A test for trypsin-like immune-reactivity in cats (fTLI) was developed to detect these. FTLI has been shown to be diagnostic for severe acute pancreatitis. However, this test is not very good in detecting milder forms of pancreatitis. A confounding factor in this test is that trypsin has been located in extra-hepatic peri-biliary glands and significant hepatic disease may lead to an increase in fTLI independent of pancreatic inflammation. Because of these limitations, the use of fTLI has fallen out of favor.
More recently, a test to measure pancreatic lipase immuno-reactivity has been developed. This test evaluates the serum for the specific lipase produced and released by the pancreas. Because of the short half-life of pancreas-specific lipase (90 minutes), continuous secretion of high levels of this enzyme into the circulation is needed for a diagnosis of pancreatitis. A quantitative assay for feline pancreatic lipase immuno-reactivity (fPLI) should be performed. Measurement of increased fPLI has been demonstrated to be a very sensitive test for detection of moderate to severe acute feline pancreatitis in cats, in which sensitivities approaching 100% have been documented. The fPLI is less sensitive in cats with mild pancreatitis, and additional studies are warranted to further evaluate the performance characteristics of this assay in cats with mild disease. Therefore, a combination of clinical suspicion, elevated fPLI, and abnormal abdominal ultrasound should be used to non-invasively diagnose acute pancreatitis
Surgery or laparoscopic biopsy for histopathology is the gold standard for diagnosis of feline acute pancreatitis. There are advantages to obtaining surgical biopsy specimens. The pancreas and peri-pancreatic area can be evaluated for abscesses and necrosis and debridement can be performed. During the procedure, a jejunostomy feeding tube can be placed, thus providing the ability to enterally feed the patient but bypassing the pancreas for digestion. The concern regarding obtaining biopsy samples from the pancreas can worsen the disease process is unfounded. However, just like other diagnostic tests for pancreatitis, biopsy has its drawbacks. The use of general anesthesia can lead to hypoperfusion of the splanchnic circulation, exacerbating the pancreatic inflammatory response. Also, pancreatitis can be a segmental disease and, since typically only 1 or 2 samples are obtained, the biopsy sample may not be representative of the process. Unless there is absolute proof of an infectious complication, which is rare, the benefit of the procedure rarely outweighs the perils of surgical intervention.