Joerg M. Steiner, Dr.med.vet., PhD, DACVIM, DECVIM-CA
Gastrointestinal Laboratory, Department of Small Animal Clinical Sciences College of Veterinary Medicine and Biomedical Sciences, College Station, TX, USA
Acute pancreatitis can be mild or severe and can be associated with systemic and/or pancreatic complications. The therapy of patients with acute pancreatitis is mainly dependant on the presence of such systemic or pancreatic complications.
Whenever possible the inciting cause should be removed. Exposure to unnecessary drugs, especially those implicated in causing pancreatitis in dogs, cats, or other species, should be avoided. Also, aggressive fluid therapy is the mainstay of supportive therapy regardless of the underlying cause of the disease process. Fluid, electrolyte, and acid-base imbalances need to be assessed and corrected as early as possible.
The traditional recommendation for any patient with 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.1 The issue is complicated further in cats by the fact that cats with pancreatitis often develop hepatic lipidosis.2 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 a nasogastric tube are acceptable alternatives if a patient does not vomit. However, in dogs or cats that do vomit the patient should be held NPO for 3-4 days.
In cats alternative routes to oral alimentation must be pursued if the cat has been anorectic before presentation or if there is evidence to support concurrent hepatic lipidosis. After holding a patient NPO water is slowly reintroduced, followed by small amounts of a carbohydrate-rich and low-fat diet.
Abdominal pain is commonly recognized in dogs but not in cats with pancreatitis.3,4 However, the presence of abdominal pain should be assumed and analgesic drugs are indicated in all small animal patients with pancreatitis. Meperidine, butorphanol tartrate, or morphine can be used parenterally. Other alternatives are a fentanyl patch or the intraabdominal administration of lidocaine.
Studies in dogs suggest that when α2-macroglobulin, one of the scavenger proteins for activated proteases in serum, is depleted death ensues rapidly. Fresh frozen plasma (FFP) and fresh whole blood not only contain α2-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 no benefit of plasma administration. However, the author believes that FFP is useful in dogs with severe forms of pancreatitis.
In contrast to human beings, infectious complications of pancreatitis are rare in dogs and cats with pancreatitis. Therefore, the use of antibiotic agents should be limited to those cases when an infectious complication can be identified or is strongly suspected.
There is no data on the use of anti-inflammatory agents in dogs and cats with severe pancreatitis, but no benefit was found in human patients. In dogs and cats with severe pancreatitis corticosteroids should only be used in secondary cardiovascular shock. Corticosteroids may be needed to treat small animal patients with IBD and concurrent pancreatitis, and do not appear to be harmful in these patients. Also, immune-mediated pancreatitis is recognized with increasing frequency in humans with pancreatitis.5 While immune-mediated pancreatitis has not been described in small animals the author believes that such a disease entity also exists in small animal patients.
Other Therapeutic Strategies
Many other therapeutic strategies, such as the administration of trypsin-inhibitors (e.g., trasylol), platelet activating factor inhibitors (PAFANTs), dopamine, antacids, antisecretory agents (i.e., anticholinergics, calcitonin, glucagon, somatostatin), or selenium, and peritoneal lavage all have been evaluated in human patients with pancreatitis. With the exception of PAFANTs and selenium, none of these 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 further evaluated before its use can be recommended.
The prognosis for dogs and cats with acute 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.
1. Williams DA, Steiner JM. Canine pancreatic disease. In: Ettinger SJ, Feldman EC. eds. Textbook of Veterinary Internal Medicine. St. Louis: Elsevier Saunders, 2005; 1482-1488.
2. Akol KG, Washabau RJ, Saunders HM, et al. Acute pancreatitis in cats with hepatic lipidosis. J Vet Int Med 1993; 7: 205-209.
3. Hess RS, Saunders HM, Van Winkle TJ, et al. Clinical, clinicopathologic, radiographic, and ultrasonographic abnormalities in dogs with fatal acute pancreatitis: 70 cases (1986-1995). J Am Vet Med Assoc 1998; 213: 665-670.
4. Washabau RJ. Acute necrotizing pancreatitis. In: August JR. ed. Consultations in feline internal medicine. St. Louis: Elsevier Saunders, 2006; 109-119.
5. Klöppel G, Lüttges J, Löhr M, et al. Autoimmune pancreatitis: Pathological, clinical, and immunological features. Pancreas 2003; 27: 14-19.