INTRODUCTION

Pancreatitis, broadly classified as acute, recurrent, or chronic, is a fairly common disease in dogs and is becoming more widely recognized in cats. ^1,2 Acute and recurrent acute pancreatitis (AP) are characterized by episodes of pancreatic inflammation with a sudden onset and variable course. Episodes may range in severity from mild and self-limiting to severe fulminant disease with extensive necrosis, systemic inflammation and/or sepsis, multiorgan failure, and death. In addition to these systemic complications, severe acute pancreatitis (SAP) (may include local complications such as pancreatic necrosis, pancreatic pseudocysts, and pancreatic abscesses.³ In veterinary medicine there is no universally accepted classification scheme for pancreatitis, with most current schemes based on variable terminology and histopathologic descriptions. However, these usually are not available at the time of diagnosis and do not necessarily correlate well with clinical severity and disease progression.^3–5 Therefore a clinically based classification system, simplified and adapted from consensus definitions in human medicine³and recently used by other authors,^1,2,6 may be more appropriate to our patient population and is used in this chapter.

PATHOPHYSIOLOGY

A number of factors have been implicated as potential etiologic factors of pancreatitis. In humans, most cases of AP are caused by biliary calculi or alcohol abuse. Most cases in dogs and cats, however, are considered to be idiopathic, because a direct causal relationship is not often demonstrated.* Regardless of the underlying etiology, AP involves intrapancreatic activation of digestive enzymes with resultant pancreatic autodigestion. Studies of animal models suggest that initial events occur within the acinar cell by abnormal fusion of normally segregated lysosomes with zymogen granules (catalytically inactive forms of pancreatic enzymes), resulting in premature activation of trypsinogen to trypsin, and may involve changes in signal transduction and increases in intracellular ionized calcium (iCa) concentrations.¹⁰ Trypsin in turn activates other proenzymes, setting in motion a cascade of local and systemic effects that are responsible for the clinical manifestations of AP.

Local ischemia, phospholipase A₂, and oxygen free radicals (produced in part from activation of xanthine oxidase by chymotrypsin) disrupt cell membranes, leading to pancreatic hemorrhage and necrosis, increased capillary permeability, and initiation of the arachidonic acid cascade. Elastase can cause increased vascular permeability secondary to degradation of elastin in vessel walls. Phospholipase A₂ degrades surfactant, promoting development of pulmonary edema, acute lung injury (ALI), and acute respiratory distress syndrome (ARDS) (see Chapter 24, Acute Lung Injury and Acute Respiratory Distress Syndrome). Trypsin may activate the complement cascade, leading to an influx of inflammatory cells and production of multiple cytokines and more free radicals. Trypsin can also activate the kallikrein-kinin system resulting in vasodilation, hypotension, and possibly acute renal failure, and the coagulation and fibrinolytic pathways, resulting in microvascular thromboses and disseminated intravascular coagulation (DIC). Local inflammation and increases in pancreatic and peripancreatic microvascular permeability may cause massive fluid losses, further compromising perfusion and stimulating additional recruitment of inflammatory cells and mediators, leading to a vicious cycle culminating in the systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) (see Chapter 11, Systemic Inflammatory Response Syndrome).

CLINICAL PRESENTATION

Clinical signs and presentation associated with AP are variable and often nonspecific, particularly in cats, and may be difficult to distinguish from those of other acute abdominal disorders. Dogs with AP are usually presented because of anorexia, vomiting, weakness, depression, and sometimes diarrhea.^12,13 They may be febrile, dehydrated, and icteric, and often exhibit signs of abdominal discomfort, sometimes with abdominal distention and absent bowel sounds from associated peritonitis and intestinal ileus. Dogs that are middle-aged and older, those that are overweight, have a history of prior or recurrent gastrointestinal (GI) disturbances, and those with concurrent endocrinopathies (diabetes mellitus [DM], hypothyroidism, or hyperadrenocorticism) have been suggested to be at increased risk for development of fatal SAP.^6,13,14 Yorkshire Terriers, Miniature Schnauzers, and other terrier breeds may also be at increased risk.^13,14 Common clinical findings in cats with AP include lethargy, anorexia, dehydration, and hypothermia; vomiting and abdominal pain appear to be reported less frequently.^15-17 Icterus and pallor often are noted as well.^4,17 Concurrent conditions such as hepatic lipidosis, inflammatory bowel disease (IBD), interstitial nephritis, DM, and cholangitis-cholangiohepatitis occur frequently, and signs of these conditions may predominate.^1,5,15-17 In either species, patients with SAP may present with signs of systemic complications including dyspnea, bleeding disorders, cardiac arrhythmias, oliguria, shock, and collapse.

DIAGNOSIS

Diagnosis of AP requires careful integration of historical, physical examination, laboratory, and diagnostic imaging findings combined with a high degree of suspicion. Because many of these findings may be nonspecific and there is wide variation in disease severity, diagnosis can be challenging. Clinicians should keep in mind that the absence of specific findings in any one diagnostic test does not rule out the possibility of AP.

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