Treatment of Canine Pancreatitis

Chapter 137

Treatment of Canine Pancreatitis

Pancreatic inflammation is a common, potentially challenging, and frustrating problem in canine internal medicine. In recent years interest in diseases of the pancreas has intensified. New diagnostic tests and imaging modalities have allowed unprecedented ability to detect pancreatic disease in canine patients. However, with this comes increasing evidence that canine pancreatic disease is far more common, and far more heterogeneous, than originally thought. With recognition of pancreatic pathology in increasing numbers of patients, determination of the correct therapeutic approach has become even more challenging. This is particularly the case in dogs with chronic pancreatic inflammation that may be either a primary disease or secondary to other gastrointestinal inflammatory disease. In some cases of chronic gastrointestinal disease with comorbid pancreatitis, the therapeutic approach may seem to be in conflict with accepted dogma regarding the treatment of pancreatitis.

Recognition of Acute Pancreatitis in the Canine Patient

The conclusive diagnosis of acute pancreatitis can be difficult. The presence of compatible clinical signs, such as vomiting, abdominal pain, dehydration, and pyrexia, increases the index of suspicion for the disease; however, no clinical findings are specific for pancreatitis.

Plain Radiography

The effects of acute pancreatitis on closely related organs and the peritoneum establish a localized peritonitis. This localized peritonitis is then the cause of most of the plain radiographic signs associated with acute pancreatitis in dogs, such as loss of contrast in the cranial abdomen, that is, the “ground glass appearance.” Plain radiographic findings are nonspecific and at best only supportive of a clinical diagnosis of acute pancreatitis. A retrospective survey of 70 fatal cases of acute pancreatitis in dogs reported radiographic findings consistent with acute pancreatitis in only 10 of 41 cases (24%) for which radiographs were available (Hess et al, 1998). Because these cases were all fatal they likely represent a biased selection toward high-severity disease (Ruaux and Atwell, 1998). The frequency of radiographic abnormalities in lower-severity cases of acute pancreatitis is likely to be low. This suggests that the negative predictive value, or the ability of negative findings on plain radiography to rule out the presence of acute pancreatitis, is low.

Measurement of Pancreatic Lipase

The broad availability of immunoassays for canine pancreas-specific lipase, in the form of the quantitative Spec cPL assay and bedside Snap cPL tests, has advanced dramatically the ability to diagnose pancreatic disease in dogs (see Chapter 135). Canine pancreas-specific lipase as a diagnostic marker for pancreatitis has received a remarkable degree of investigation in the peer-reviewed literature and has been shown to have high sensitivity and specificity by several different groups and in a variety of contexts (Neilson-Carley et al, 2011; Trivedi et al, 2011). In an animal with compatible clinical signs, the presence of an elevated pancreas-specific lipase concentration provides strong evidence to support the clinical diagnosis of pancreatitis, whereas a normal concentration in a dog with similar signs is a strong indication that pancreatic disease is not present and should prompt investigation for other differential diagnoses.

Pathophysiology of Acute Pancreatitis

The pathophysiology of acute pancreatitis at the level of the exocrine cell, including changes in digestive enzyme handling and secretion, has been reviewed earlier (see page 534 of the previous edition of Current Veterinary Therapy). Although changes in the exocrine cell are important and have been investigated extensively in a variety of canine and rodent models of the disease, the relationship between these changes and the clinical outcome of naturally occurring pancreatic disease is tenuous at best. A growing body of evidence suggests that the exocrine pancreas is a source of numerous inflammatory cytokines during a bout of acute pancreatitis, and the systemic effect of these cytokines is the major determinant of overall severity and likelihood of complications in these cases. Severe acute pancreatitis puts the patient at a high risk for systemic inflammatory response syndrome (SIRS), which can then lead to multiple organ dysfunction syndrome (MODS) and death. The processes of SIRS and MODS, once initiated, tend to continue independent of the triggering factor. A rational therapeutic approach to these cases, then, is aimed at preempting complications and managing complications that can arise as a result of systemic inflammation. Early, aggressive therapy is important to prevent complications from acute pancreatitis. It is important to articulate to dog owners the need for this early, aggressive therapy and the likelihood of severe and significant complications early in the course of treating the disease.

Therapy of Acute Pancreatitis

Fluid Therapy

Fluid therapy is absolutely central to the management of most cases of acute pancreatitis in dogs, particularly those judged to be sufficiently severe to warrant hospitalization. For most cases of uncomplicated pancreatitis (those without accompanying organ failures), therapy with a replacement-type crystalloid intravenous fluid (typically supplemented to contain 20 to 30 mEq/L potassium) is sufficient. The volume of fluid given should be based on careful estimation and calculation of fluid deficits and maintenance needs. A typical aim is to replace calculated deficits over 8 to 12 hours, following a 30-minute to 1-hour period of shock rate fluid delivery (70 to 90 ml/kg/hr). The patient then is maintained at up to twice the calculated maintenance rate with crystalloid fluids once the fluid deficit is replaced, while urine output is monitored. This rate of fluid administration is continued until the animal is drinking and decreased to the maintenance rate at this point. Dogs with acute pancreatitis commonly are potassium depleted because of losses from vomiting, effective loss of circulating volume in bowel loops because of ileus, and enhanced renal potassium losses. Close monitoring of electrolytes (typically every 12 hours) and judicious supplementation are indicated in the initial period of fluid resuscitation.

In dogs with more severe acute pancreatitis the impact of systemic circulation of pancreas-derived inflammatory mediators becomes important. Although severe cases still demonstrate the fluid losses and electrolyte disturbances common in the less severe examples of pancreatitis, additional complicating factors arise as a result of vascular endothelial dysfunction.

Systemic vascular endothelial dysfunction from inflammation is associated with an increased rate of fluid loss into the extracellular spaces of tissues. This deterioration in endothelial function means a tendency for losses of albumin and lower-molecular-weight plasma proteins from circulation and into the extracellular space. The net effect of this is a loss of the plasma’s colloid oncotic pressure and thus a declining ability to maintain circulating fluid volume and cardiac output. Colloid replacement, as part of the initial fluid resuscitation and for ongoing maintenance, commonly is indicated in more severe cases of acute pancreatitis.

Fresh frozen plasma (aiming for 10 to 15 ml/kg in the initial transfusion) is the author’s preferred colloid fluid in the management of severe acute pancreatitis, particularly in the initial stages of volume replacement and fluid resuscitation. Fresh frozen plasma provides colloid support via replacement of albumin and other high-molecular-weight proteins, as well as replacing clotting factors and anti-thrombin III. Dogs with severe acute pancreatitis are at risk for the development of disseminated intravascular coagulation, and preemptive replacement of clotting factors and clotting cascade moderators is indicated. Although the use of fresh frozen plasma is the author’s first choice for colloid support in dogs with severe acute pancreatitis, there is a lack of well-controlled studies demonstrating efficacy in canine patients with pancreatitis, and some retrospective studies have called into question the usefulness of this therapy (Weatherton and Streeter, 2009).

For cases requiring longer-term colloid support, particularly in which owner finances are limiting, synthetic colloids such as hetastarch can be administered (a total of 10 to 20 ml/kg q24h IV, with an initial bolus of half this volume given over 30 minutes followed by the balance as a continuous rate infusion [CRI]).

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Treatment of Canine Pancreatitis
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