The incidence of exocrine pancreatic disorders has traditionally been considered to be low in the cat. However, in a large retrospective study of necropsy findings 1.3% of 6,504 feline pancreata showed significant pathological lesions.(1) This frequency of lesions of the exocrine pancreas at necropsy in cats compares to 1.5% reported in 9,342 pancreata from dogs.(1) Clinical findings stand in sharp contrast to these findings during necropsy. Of 180,648 cats entered into the Veterinary Medical Data Base (VMDB) at Purdue University over a ten-year period, only 1,027 or 0.57% were diagnosed with exocrine pancreatic disorders.(2) Thus, while cats suffer from diseases of the exocrine pancreas quite frequently, these disorders often escape definitive diagnosis. Approximately 50% of all cats with exocrine pancreatic disorders have pancreatitis, 2/3 of which are chronic and 1/3 acute.(3) According to the current classification system of human pancreatitis acute pancreatitis is an inflammatory condition of the pancreas that is completely reversible after removal of the inciting cause.(4) Chronic pancreatitis is characterized by irreversible histopathologic changes such as fibrosis of exocrine pancreatic tissue. Both forms can be mild or severe depending on systemic involvement. Mild forms of pancreatitis are associated with no or little pancreatic necrosis and systemic effects and often allow recuperation of the patient. In contrast, severe forms of pancreatitis are associated with extensive pancreatic necrosis, multiple organ involvement, and often a poor prognosis.
Etiology and Pathogenesis
It is believed that all pancreatitis is caused by a common pathophysiologic pathway. Pancreatic acinar cells respond to any number of different insults by a decreased secretion of pancreatic enzymes, co-localization of zymogen granules and lysosomes, premature activation of trypsin, and subsequently of other digestive zymogens.(5) These activated digestive enzymes cause local effects, such as inflammation, hemorrhage, acinar cell necrosis, and peripancreatic fat necrosis. Digestive enzymes released into the blood stream may cause systemic effects, including systemic inflammatory changes, systemic vasodilatation leading to hypotension, pulmonary edema, disseminated intravascular coagulation, central neurologic deficits, respiratory failure, renal failure, and multiorgan failure. However, over the last decade there has been convincing evidence that at least in part systemic effects and progression of pancreatitis are due to release of cytokines.(6)
Several diseases and risk factors have been associated with feline pancreatitis.(7,8) Traumatic pancreatitis (hit by cars or high-rise syndrome) has been reported.(7,9) Surgical trauma can cause pancreatitis but many human patients that undergo surgery of organs distant from the pancreas have been shown to be at an increased risk for pancreatitis suggesting that hypoperfusion of the exocrine pancreas during anesthesia may be of bigger importance than surgical handling of the organ itself. Infectious agents have been shown to cause feline pancreatitis, with the strongest causal relationship for Toxoplasma gondii, and rare cases of Amphimerus pseudofelineus infestation.(10) Weaker evidence has been presented for feline panleukopenia virus infections in kittens and infections with Feline Herpesvirus I and feline infectious peritonitis virus. Two cases of feline pancreatitis after topical use of fenthion, an organophosphate cholinesterase inhibitor, have been reported.(7) More than drugs or drug groups have been implicated in causing pancreatitis in human beings and drug-induced pancreatitis has also been reported in dogs, but no cases have been reported in the cat.(11) Cholangitis and cholangiohepatitis may coexist in feline patients with pancreatitis, but there is no evidence that they play a causative role in this disease. Unfortunately, it appears that more than 90% of all cases of feline pancreatitis are idiopathic.
Clinical Picture and Diagnosis
Clinical signs of cats with pancreatitis are nonspecific. In a report of 40 cats with severe forms of pancreatitis lethargy was reported in 100% of these cases, anorexia in 97%, dehydration in 92%, hypothermia in 68%, vomiting in 35%, abdominal pain in 25%, a palpable abdominal mass effect in 23%, dyspnea in 20%, ataxia in 15%, and diarrhea also in 15%.(7) Especially remarkable is the low incidence of vomiting and abdominal pain, both of which are common clinical signs in human and canine pancreatitis patients. Other clinical signs, such as polyphagia, constipation, fever, icterus, polyuria, polydipsia, and adipsia have also been reported. Concurrent conditions occur frequently, including hepatic lipidosis, inflammatory bowel disease (IBD), interstitial nephritis, diabetes mellitus, and cholangiohepatitis.(12) Complete blood count and serum chemistry profile often show mild and nonspecific changes.(7) Serum activities of lipase and amylase are within the reference range in almost all cases.(13) Radiographic changes seen in some cases include a decreased contrast in the cranial abdomen and displacement of abdominal organs with the duodenum displaced laterally and dorsally, the stomach to the left, and the transverse colon caudally. Abdominal ultrasound is useful in the diagnosis of feline pancreatitis but its usefulness is largely operator-dependant. Changes identified include pancreatic enlargement, hypoechogenicity in cases of pancreatic necrosis, hyperechogenicity in cases of pancreatic fibrosis, hyperechogenicity of peripancreatic fat, fluid accumulation around the pancreas, and less frequently a mass effect in the area of the pancreas.(14) Abdominal computed tomography is a routine procedure in humans suspected of having pancreatitis, but appears to be very insensitive for the diagnosis of pancreatitis in the cat. Measurement of feline trypsin-like immunoreactivity in cat serum (fTLI) is currently only available through the GI Laboratory at Texas A&M University.(15) Initial studies indicate that a serum fTLI > 100 mg/L is approximately 80–90% specific and 30–60% sensitive for feline pancreatitis.(13,16) This test is by no means an ideal test for feline pancreatitis, but it is the most clinically useful test currently available.(17) Integration of clinical data, clinical pathology and imaging findings, and measurement of serum fTLI concentration appears to be most useful clinically. A definitive diagnosis of feline pancreatitis can often only be made by pancreatic biopsy at exploratory laparotomy or laparoscopy. However, this may be cost-prohibitive in some cases and many cats especially with severe forms of pancreatitis may be poor anesthetic risks.
Whenever possible the inciting cause should be removed. Exposure to unnecessary drugs, especially those implicated in causing pancreatitis in cats (organophosphates) or other species, should be avoided. Aggressive fluid therapy is the mainstay of supportive therapy. Fluid, electrolyte, and acid-base imbalances need to be assessed, and corrected on a continuous basis.
The traditional recommendation for any patient suffering from pancreatitis is to give nothing per os for three to four days. This recommendation is justified in patients that vomit, but there is little evidence to justify this strategy in patients that do not. The issue is complicated further by the fact that cats with pancreatitis often concurrently suffer from hepatic lipidosis.(12) Preferred routes of alimentation are a jejunostomy tube or total parenteral nutrition. However, these strategies are impractical in many cases and a gastrostomy tube or even a nasogastric tube is an acceptable alternative if the patient does not vomit. However, if the patient does vomit or the cat has not been anorectic before presentation and there is no evidence to support concurrent hepatic lipidosis, the cat should be held NPO for three to four days. After this time water is slowly reintroduced, followed by small amounts of a carbohydrate-rich, low-fat diet.
Abdominal pain is uncommonly recognized in cats with pancreatitis. However, if abdominal pain is thought to be present, analgesic drugs are indicated. Meperidine at a dose of 1.0–2.0 mg/kg q2–4h or butorphanol tartrate at a dose of 0.2–0.4 mg/kg q6h can be given subcutaneously. In many feline patients abdominal pain is only diagnosed after significant clinical improvement is recognized after analgesic therapy.
Studies in dogs suggest that when alpha-2-macroglobulin, one of the scavenger proteins for activated proteases in serum, is depleted, death ensues rapidly. Fresh frozen plasma (FFP) or fresh whole blood not only contain alpha-2-macroglobulin, but also albumin, which has many beneficial effects in patients suffering from severe pancreatitis. In clinical trials in human patients with acute pancreatitis there was little evidence of any benefit of plasma administration. However, many veterinary clinicians feel that small animal patients with severe pancreatitis benefit from plasma administration.
In contrast to humans, infectious complications of pancreatitis are rare in cats. Therefore, the use of antibiotic agents should be limited to those cases when an infectious complication can be identified or is heavily suspected.
There is no data on the use of anti-inflammatory agents in cats suffering from severe pancreatitis. No benefit was found in human patients. In cats with severe pancreatitis, corticosteroids should only be used in cases of secondary cardiovascular shock. However, corticosteroids may be needed to treat cats with IBD and concurrent mild chronic pancreatitis, and do not appear to be harmful in these patients.
Many other therapeutic strategies, such as the administration of trypsin-inhibitors (e.g., trasylol), platelet activating factor inhibitors, dopamine, antacids, antisecretory agents (i.e. anticholinergics, calcitonin, glucagon, somatostatin), or selenium, and peritoneal lavage all have been evaluated in human patients suffering from pancreatitis. With exception of platelet activating factor inhibitors and selenium, none of these strategies have shown any beneficial effect at this point. The efficacy of selenium, which has also been shown to decrease mortality in dogs with pancreatitis in an uncontrolled study, needs to be evaluated in cats with pancreatitis.
It should also be remembered that many cats have mild forms of chronic pancreatitis. Often times these cats suffer from concurrent conditions, most notably IBD. Very little is known about appropriate therapy for these animals, and management is often limited to evaluation and treatment of the concurrent condition, and careful monitoring of pancreatic inflammation. Just as human patients with chronic pancreatitis these cats are at risk of developing exocrine pancreatic insufficiency later in life.
The prognosis for cats suffering from severe pancreatitis is directly related to disease severity, extent of pancreatic necrosis, occurrence of systemic and pancreatic complications, duration of the condition, and the presence of concurrent disease.
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