A criticalist's view of canine pancreatitis (Proceedings)
Many canine patients present to the veterinarian with vomiting, diarrhea, anorexia, and abdominal discomfort, with or without fever. Based on these non-specific signs of disease, the veterinarian has to build a differential diagnosis list. This list commonly includes acute gastro-enteritis (parasitic, bacterial, viral), dietary indiscretion/foreign body ingestion, toxicity, renal disease, pancreatitis, hypoadrenocorticism, and cholangiohepatitis, among others. The job of the veterinary clinician is to determine which of these disease processes are involved in the patient's illness and then determine the best course of therapy for the patient. The goals of this lecture are to help the veterinarian differentiate pancreatitis from the other disease processes listed above and then determine what traditional and ancillary therapies are warranted in treating the patient with acute pancreatitis.
Pathophysiology of Acute Pancreatitis
Many different inciting causes have been postulated to cause canine acute pancreatitis. High fat diets and dietary indiscretions are the most common clinically quoted causes of pancreatitis. Yet, there is little scientific evidence for these etiologies. The use of corticosteroids has also been quoted as an underlying cause. Corticosteroid use in dogs causes serum lipase activity to increase. However, several studies have shown no pancreatic lesions in animals receiving corticosteroids; the lipase must be another type of lipase. However, a lot of patients receiving steroid therapy have diseases that predispose them to pancreatitis, so the primary disease process may be at fault, not the steroids administered to treat those diseases. Etiologies that have been shown to cause pancreatitis include certain drugs, most commonly potassium bromide, hypercalcemia, hyperlipidemia, especially in miniature Schnauzers, pancreatic hypoperfusion from general anesthesia or hypovolemia, and trauma. Immune-mediated disease, common in the human population with pancreatitis, may play a role in many of the canine patients with pancreatitis, although this has yet to be studied.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 or ascending infection up the pancreatic duct. 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.
Histologically, acute pancreatitis is characterized by findings that range from pancreatic edema to necrosis, variable infiltrates of mononuclear and polymorphonuclear cells, and local changes such as peri-pancreatic fat necrosis and thrombosis. Acute pancreatitis may resolve or persist and can be complicated by secondary infection and pseudocyst or abscess formation. It is tempting to equate mild acute pancreatitis with pancreatic edema, and severe or fatal pancreatitis with pancreatic necrosis, but this relationship has not been critically examined in patients with naturally occurring pancreatitis