Pancreatitis: Overview - The Merck Veterinary Manual

Pancreatitis: Overview

Pancreatitis is the most common exocrine pancreatic disease in both dogs and cats. It can be acute or chronic, depending on whether or not the disease has led to permanent changes of the pancreatic parenchyma. Both acute and chronic pancreatitis can be severe and associated with pancreatic necrosis and systemic complications. Thus a distinction between the two is clinically of little significance.

Etiology and Pathogenesis:

Most cases of pancreatitis in dogs and cats are idiopathic. However, dietary indiscretion is believed to be a common risk factor in dogs. Severe trauma or surgery can also lead to pancreatitis. However, anesthesia-induced hypotension may be more important in inducing pancreatitis than trauma from handling of the pancreas. Infectious diseases have been implicated, but the evidence for a cause and effect relationship is weak, except for Toxoplasma gondii and Amphimerus pseudofelineus in cats. Many drugs have been implicated in causing pancreatitis in humans but very few have been confirmed in dogs and cats. In general, most drugs should be viewed as potential causes of pancreatitis; anticholinesterases, calcium, L-asparaginase, estrogen, salicylates, azathioprine, thiazide diuretics, and vinca alkaloids are probably the most likely. Corticosteroids were long considered to be a risk factor for pancreatitis but have recently been removed from the list of drugs that may induce pancreatitis in humans. Similarly, there is no credible evidence that corticosteroids are a risk factor for pancreatitis in dogs or cats.

Many different insults may ultimately lead to pancreatitis through a common mechanism. Secretion of pancreatic juice decreases during the initial stages of pancreatitis. This is followed by localization of both zymogen granules and lysosomes, leading to activation of trypsinogen. Trypsinogen in turn activates more trypsinogen and also other zymogens. Prematurely activated digestive enzymes lead to local damage of the exocrine pancreas with pancreatic edema, bleeding, inflammation, necrosis, and peripancreatic fat necrosis. The inflammatory process also leads to recruitment of WBC and cytokine production. The activated enzymes, and more importantly, the cytokines circulate in the bloodstream and lead to distant complications such as generalized inflammation, disseminated intravascular coagulation, disseminated lipodystrophy, pancreatic encephalopathy, hypotension, renal failure, pulmonary failure, or even multiorgan failure.

Clinical Findings:

Anorexia (91%), vomiting (90%), weakness (79%), abdominal pain (58%), dehydration (46%), and diarrhea (33%) are the most common clinical signs reported in dogs with severe pancreatitis. Clinical signs in cats with severe pancreatitis are even less specific with lethargy (100%), anorexia (97%), dehydration (92%), hypothermia (68%), vomiting (35%), and abdominal pain (25%) most commonly reported. The low rate of abdominal pain reported is remarkable given that >90% of human patients with pancreatitis report abdominal pain.

Diagnosis:

A history of dietary indiscretion combined with vomiting and abdominal pain may suggest pancreatitis in dogs, but most cats present with nonspecific histories and clinical signs. Findings on CBC and serum biochemistry profiles may suggest an inflammatory disease process but are nonspecific. In dogs, thrombocytopenia and neutrophilia with a left shift are common. Azotemia and elevations in liver enzymes and bilirubin are common, nonspecific findings in both dogs and cats. Abdominal radiographs may show decreased detail in the proximal abdominal cavity and displacement of abdominal organs, but these findings are also nonspecific and a diagnosis based on radiographic findings alone is not reliable. Abdominal ultrasound, if stringent criteria are applied, is highly specific for pancreatitis, but pancreatic enlargement and fluid accumulation around the pancreas alone are not sufficient for diagnosis. A combination of pancreatic enlargement, fluid accumulation around the pancreas, changes in echogenicity (decreased echogenicity in cases of pancreatic necrosis, increased echogenicity in cases of fibrosis), and/or a pancreatic mass effect are highly specific for pancreatitis. Unfortunately, the sensitivity of abdominal ultrasound is highly operator-dependent, with sensitivities as high as 35% in cats and 65% in dogs in the most experienced hands.

Several diagnostic markers for pancreatitis have been evaluated in dogs and cats. Serum lipase and amylase activities have limited clinical usefulness in dogs and no usefulness in cats. In dogs with suspected pancreatitis, serum amylase and lipase can be used as a diagnostic indicator until a more definitive diagnostic test (eg, abdominal ultrasonography or serum pancreatic lipase immunoreactivity [PLI] concentration) can be performed. Serum trypsin-like immunoreactivity (TLI) concentration is also of limited clinical usefulness for the diagnosis of pancreatitis in dogs. Although highly specific for exocrine pancreatic function, it has a sensitivity of only 30-60%, depending on the study. In both dogs and cats, serum PLI concentration is highly specific for exocrine pancreatic function and is also the most sensitive currently available diagnostic test for pancreatitis (sensitivity >80%). The canine and feline PLI assays are currently performed only by the GI Laboratory at Texas A&M University.

Abdominal exploratory laparotomy can also be used to definitively diagnose pancreatitis. However, even if the presence of pancreatitis seems obvious (eg, pancreatic congestion can easily be misdiagnosed as pancreatitis on gross examination), a biopsy specimen should be collected, as the definitive diagnosis of pancreatitis requires the identification of an inflammatory infiltrate. It is difficult to exclude pancreatitis during abdominal exploratory laparotomy. In many cases, pancreatitis is localized to one lobe of the pancreas and may be missed when a single biopsy is being collected. Also, patients with severe pancreatitis are often poor anesthetic risks, and exploratory laparotomy may not be justified.

Treatment:

The mainstay of therapy is supportive care with fluid therapy, vigorous monitoring, and early intervention to prevent systemic complications. In those few cases in which the etiology is known, specific therapy against the inciting cause may be initiated. Antibiotics are of questionable value. Resting the exocrine pancreas by giving the patient nothing per os (NPO) for 3-4 days is still recommended in most cases, although the validity of this approach has been questioned. Patients that vomit may be held NPO. However, patients held NPO should be given alternative nutritional support. This is especially important in cats that are at risk for secondary hepatic lipidosis. Total parenteral nutrition and jejunostomy tubes have both been suggested. However, these are often not feasible in a general practice setting; nasogastric and gastric tubes may be viable alternatives in patients that are not vomiting incessantly. Abdominal pain should be assumed to be present and treated until contrary evidence is available. Traditionally, meperidine and butorphanol have been used, but many opioids, such as fentanyl or morphine are also useful. Intra-abdominal lidocaine has also been used. Plasma appears to be helpful in severe cases of canine pancreatitis. It should be given daily until improvement is significant or until adverse effects are identified. Many other treatments have been investigated in dogs, cats, and humans, but unfortunately none has been shown to be useful.

Prognosis:

The prognosis in mild cases is good, but prognosis in severe cases of pancreatitis is poor in both dogs and cats. About 50% of human patients with severe pancreatitis die, and the mortality rate appears to be similar in dogs and cats. A challenge in both human and veterinary medicine is the identification of severe cases early during the disease process and the prevention of complications.