Current status of treatment for pancreatitis

NUTRITIONAL MANAGEMENT OF PANCREATITIS IN DOGS

Historically, it has been advocated to “rest” the pancreas during bouts of acute pancreatitis by withholding enteral nutrition to avoid stimulation of the exocrine pancreas and the risk for continued premature zymogen activation.3-6 Supporting evidence for this practice is minimal, and several studies challenge it.6 Evidence is mounting that early enteral nutrition improves clinical outcomes in systemically ill patients.3,4,7,8 Specifically, early enteral nutrition has been shown to decrease ileus and inflammation, stimulate intestinal mucosal regeneration and mucosal blood flow, decrease protein catabolism, and prevent protein-energy malnutrition.4,6,9 A recent retrospective study of 34 dogs with acute pancreatitis concluded that early enteral nutrition (i.e., within 48 hours of hospitalization) had a positive effect on return to voluntary food intake, was associated with less gastrointestinal intolerance, and should be considered as part of medical management.4

Imposed anorexia may be counterproductive to overall gastrointestinal health, as avoidance of enteral nutrition has been correlated with increased gastrointestinal permeability, bacterial or endotoxin translocation, and immunosuppression.3,6,10 Increased metabolic demands, protein catabolism, and bacterial translocation associated with pancreatitis itself may lead to systemic inflammatory response syndrome (SIRS).10

INTRAVENOUS FLUID THERAPY

A disturbance in pancreatic microcirculation plays a central role in the pathogenesis of acute pancreatitis and the transformation from acute, self-limiting to severe, necrotizing pancreatitis.1,3,19 The pancreatic microcirculation can be disturbed by many factors, including hypovolemia, dehydration, increased capillary permeability, and microthrombi.1,3,19

The rationale for intravenous fluid therapy is to replenish blood volume and thus blood flow to the pancreas, with several animal studies demonstrating both improved pancreatic circulation and survival with fluid resuscitation.20,21 However, pancreatic blood flow and oxygen consumption are not completely restored with fluid resuscitation alone.21 Little information is available pertaining to the best initial fluid choice; however, an isotonic fluid (e.g., lactated Ringer’s solution, 0.9% sodium chloride) is appropriate. The fluid plan should incorporate the estimated fluid deficit, any ongoing losses (i.e., vomiting, diarrhea), and the ongoing maintenance requirement. Electrolytes should be monitored and supplemented accordingly.

Glucocorticoids

Historically, the use of glucocorticoids has been avoided in dogs with acute pancreatitis.26 Glucocorticoids are no longer believed to cause pancreatitis in dogs;1,3 however, there is currently no consensus with regard to their use or optimum timing/dose in patients with pancreatitis.

Glucocorticoids counteract nearly all pathways of inflammation.26 In pancreatitis, they have been shown to enhance apoptosis and increase the production of pancreatitis-associated proteins, which confer a protective effect against pancreatic inflammation.3,26 A recent clinical study demonstrated that dogs receiving prednisolone 1 mg/kg/day had a greater decrease in C-reactive protein concentration, fewer days until clinical improvement, shorter hospitalization periods, and better survival.26 Conclusions from these studies should be viewed with caution and other facets of aggressive medical management of pancreatitis should be maximized before the implementation of glucocorticoid therapy. Further objective clinical trials are needed to confirm findings from the most recent studies.

Antibiotics

Antibiotic treatment for acute pancreatitis is not recommended, as pancreatitis is considered to be a sterile inflammatory process that is often accompanied by pyrexia and leukocytosis.1 Indications for the use of antibiotics include failure to respond to aggressive supportive care, pancreatic necrosis with secondary infection/abscessation, or melena and hematochezia suspected to be caused by bacterial translocation from the small intestine.1,27 When indicated, broad-spectrum parenteral antibiotics that are effective against gastrointestinal pathogens (e.g., amoxicillin-clavulanate) should be considered.1

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