Pancreatitis in the Cat
World Small Animal Veterinary Association World Congress Proceedings, 2015
M. Costello1, DVM, DACVECC
1VCA Boston Road Animal Hospital, Springfield, MA, USA

Feline pancreatitis is a multifaceted disease that can result in severe and potentially fatal systemic inflammation and comorbidities. The systemic inflammation and concurrent diseases, such as hepatic lipidosis, diabetes, biliary duct obstruction, can result in organ dysfunction and failure that can be fatal in some patients. It has been clearly documented that there are significant differences in the feline response to critical illness.

Feline pancreatitis has been classified into many different categories. One classification scheme divides pancreatitis into acute, chronic active, and chronic. Within this classification acute is further broken down into acute necrotizing and acute suppurative. Clinically, pancreatitis can be classified as mild or severe based on the severity of secondary systemic effects, pancreatic necrosis and mortality.

The unique physiology in cats is also related to the clinical manifestations of pancreatitis. Unlike dogs, the majority of cats (80%) have only one pancreatic duct, as the accessory pancreatic duct generally does not persist after development. The pancreatic duct in the cat enters the duodenum through the major duodenal papilla, alongside the bile duct. Pancreatic secretion is mediated both through neural as well as hormonal mechanisms. In cats, the primary mechanism is thought to be hormonal, mediated by secretin and cholecystokinin (CCK) which are released when food enters the small intestine.

Pancreatitis in cats can be the primary disease manifestation or it can occur secondary to disease in other areas of the body. Determination of the exact inciting event is often difficult, if not impossible. In a study of 40 cases of acute necrotizing pancreatitis and suppurative pancreatitis in the cat, the authors report that most cats had no clear etiology. Pancreatic disease has been associated with dysfunction of numerous organs, including liver/hepatobiliary, endocrine pancreas (diabetes, diabetic ketoacidosis), kidneys, intestines, lungs, and peritoneum (effusion). Traumatic injury, surgery, drugs, toxic (organophosphate) and infectious causes have also been implicated. Regardless of the underlying or inciting event, the development of pancreatitis is generally thought to be secondary to a failure of the inherent protective mechanisms of the pancreas. This failure results in zymogen activation within the pancreas and subsequent entry into the interstitium and peritoneal cavity. This leads to local inflammation, pancreatic tissue damage and cell death. The severity of the local and subsequent systemic inflammation is regulated by plasma protease inhibitors in the circulation. The main circulating inhibitors are α1-protease inhibitor and α-macroglobulins. Exhaustion of these protective mechanisms can lead to systemic inflammation and secondary organ dysfunction. Depending on the organ system affected, the systemic sequelae of pancreatitis may include diabetes/DKA, renal failure, disseminated intravascular coagulation, hepatic dysfunction, bile duct obstruction, acute respiratory distress syndrome, myocardial dysfunction, sepsis or death.

Unfortunately, the clinical signs seen in cases of feline pancreatitis are often vague and nonspecific. Clinical signs frequently associated with pancreatitis in cats include lethargy, anorexia, dehydration, tachypnea, hypothermia, and icterus. In one study, only 35% of cats had a history of vomiting, and only 25% had reported abdominal pain. In addition, clinical signs are often confounded by the presence of one or more comorbid conditions (e.g., diabetes, inflammatory bowel disease, hepatic lipidosis). Routine diagnostic testing, although essential for evaluation of other organ systems, often provides little assistance in the diagnosis of pancreatitis. This absence of pathognomonic clinical or clinicopathologic signs may explain the fact that antemortem diagnosis of pancreatitis in the cat is rare.

As previously stated, the clinicopathologic changes seen in these cats are typically indistinguishable from those seen in other diseases associated with critical illness. Despite this lack of sensitivity, routine bloodwork is an essential part of the work-up in these cats. Abdominal ultrasound plays an integral role in evaluating not only the pancreas in affected cats, but also other intraabdominal organs. Although CT is useful in people with pancreatitis, it has limited diagnostic utility in our feline patients. In addition, more specialized testing has been investigated to try and improve antemortem diagnosis.

Complete blood count and serum chemistry profile are in general consistent with a critically ill cat nonspecific for underlying cause. The changes in the chemistry profile are often related to dysfunction in other organ systems. Hypocalcemia is a common finding in cats with pancreatitis, and a low plasma ionized calcium concentration (< 1 mmol/l) has been associated with a greater morbidity and mortality in cats with acute pancreatitis. Although helpful in humans and dogs, pancreatic enzymes (amylase, lipase) are poor indicators of pancreatic disease in the cat. They are frequently normal despite significant disease and amylase has actually been shown to decrease in experimental models of pancreatitis in the cat. In two studies of naturally occurring pancreatitis in cats, 4/4 and 12/12 cats had normal serum amylase concentrations. Coagulation times (prothrombin time, partial thromboplastin time) may be elevated in cats with severe systemic inflammation and secondary organ failure.

On imaging (radiographs, abdominal ultrasound), neither of these tests are specific or sensitive for pancreatic disease. Considerable expertise and experience are required to definitively identify changes in the feline pancreas on abdominal ultrasound, and the sensitivity of this test has previously been reported to be very low (24%). However, in a more recent study, abdominal ultrasound was found to be 80% sensitive in cats with moderate to severe pancreatitis.

In humans, CT is a standard tool used in the diagnosis of pancreatitis. However, in a study evaluating diagnostic tests for pancreatitis in cats, the sensitivity of this test was extremely low (20%).

Feline pancreatic lipase immunoreactivity (fPLI) has recently been validated for use in cats. A prospective study was done evaluating fPLI versus other diagnostic tests in cats with and without pancreatitis. fPLI was reported to be 100% sensitive in cats with moderate to severe pancreatitis, and 100% specific in healthy cats. The high sensitivity and specificity of this test suggest that it may play a significant role in the noninvasive diagnosis of feline pancreatitis. In a study evaluating serial serum feline pancreatic lipase immunoreactivity concentrations and prognostic variables in 33 cats with pancreatitis, the authors found that dyspnea, hyperkalemia, and serum fPLI concentration at the time of hospital admission were significant prognostic factors for cats hospitalized because of pancreatitis.

The treatment for the cat with pancreatitis is primarily supportive care, and therapy for organ dysfunction. Dehydration is common in these cats, and fluid therapy should be aimed at replacing deficits, providing maintenance requirements, and providing for any ongoing losses. In cats with hypotension, the shock bolus is 50–60 ml/kg of crystalloids or 5 ml/kg of colloids. It is important to remember, though, that fluid therapy must be used judiciously, as critically ill cats are predisposed to fluid overload, pulmonary edema and pleural effusion. In some cats, hypotension remains despite adequate volume. In these cases, exogenous catecholamine therapy is necessary.

Although not a common finding in cats with pancreatitis, vomiting can occur either due to pancreatitis or dysfunction in other organ systems. In these cats, antiemetics such as metoclopramide, prochlorperazine or ondansetron should be administered.

Unlike dogs, fasting is not recommended in cats with pancreatitis unless the patient is vomiting. Hepatic lipidosis is a common problem in these cases, and alimentary support is an integral component of treatment. Ideally, nutrition is provided enterally. This can be accomplished via a nasoesophageal tube, percutaneous gastrotomy tube, or a jejunostomy tube. In a study evaluating nasogastric tube feeding (NGT) in 55 cases of suspect acute pancreatitis, NGT was well tolerated and associated with a low incidence of diarrhea, vomiting, and mechanical complications.

Routine use of antibiotics in cats with pancreatitis is quite controversial. Studies in humans have failed to show beneficial effects of routine antibiotic use but experimental work in cats has documented that bacterial flora are able to colonize an inflamed pancreas from multiple sources, including the colon.

Pain can be difficult to assess in these cats, and the severity of clinical signs can sometimes result in a reluctance of clinicians to treat with pain medications. Analgesics such as buprenorphine (5–10 mcg/kg) or butorphanol (0.2–0.4 mg/kg) can be administered to treat abdominal pain associated with pancreatitis and potential peritonitis. Other possible options include fentanyl (continuous rate infusion, fentanyl patch) or epidural analgesia.

Cats with acute pancreatitis are dynamic cases and careful monitoring is vital to the management of these cats. Indirect monitoring of blood pressure as well as central venous pressure monitoring can help guide therapy in these cats, and pulse oximetry is a noninvasive method to evaluate oxygen saturation and monitor respiratory status.

The prognosis for pancreatitis in the cat is directly related to the severity of pancreatic disease as well as the present of concurrent organ dysfunction. In a recent report of 46 cases of acute pancreatitis the fatality rate was 41%. Aggressive supportive care is imperative to maximize the chances for recovery in these cats.

References

References are available upon request.

  

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

M. Costello, DVM, DACVECC
VCA Boston Road Animal Hospital
Springfield, MA, USA


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