Diagnostics , Hepatology

Feline Acute Pancreatitis: Current Concepts in Diagnosis and Therapy

Feline Acute Pancreatitis: Current Concepts in Diagnosis and Therapy
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P. Jane Armstrong, DVM, MS, MBA, Diplomate ACVIM, and Sarah Crain, DVM, MS, Diplomate ACVIM

Pancreatitis appears to be a common disease in cats,1 yet it remains frustratingly difficult to establish a clinical diagnosis with certainty. Clinicians must rely on a combination of compatible clinical findings, serum feline pancreatic lipase (fPL) measurement, and ultrasonographic changes in the pancreas to make an antemortem diagnosis, yet each of these 3 components has limitations.

Fel Acute Pancr Fig 1

FIGURE 1. Duodenum (D) and duodenal limb of the pancreas (P) in a cat with acute pancreatitis and necrosis; well-demarcated areas of necrosis are present at the periphery of the pancreas in the peripancreatic adipose tissue(arrows). Courtesy Dr. Arno Wuenschmann, Minnesota Veterinary Diagnostic Laboratory

PROFILE

Acute Versus Chronic Pancreatitis

Acute pancreatitis is characterized by neutrophilic inflammation, with variable amounts of pancreatic acinar cell and peripancreatic fat necrosis (Figure 1).1 Evidence is mounting that chronic pancreatitis (see In Brief: Diagnosis & Treatment of Feline Chronic Pancreatitis) is more common than the acute form, but sonographic and other clinical findings overlap considerably between the 2 forms of disease.1-3

Diagnostic Challenges

Use of histopathology as the gold standard for diagnosis has recently been questioned because of the potential for histologic ambiguity.3,4 A seminal paper exploring the prevalence and distribution of feline pancreatic pathologic abnormalities reported that 45% of cats that were apparently healthy at time of death had histologic evidence of pancreatitis.1 The 41 cats in this group included cats with no history of disease that died of trauma, and cats from clinical studies that did not undergo any treatment (control animals). Conversely, multifocal distribution of inflammatory lesions was common in this study, raising the concern that lesions could be missed on biopsy or even necropsy.

Prevalence

Such considerations help explain the wide range in the reported prevalence of feline pancreatitis, from 0.6% to 67%.3 The prevalence of clinically relevant pancreatitis undoubtedly lies somewhere in between, with acute and chronic pancreatitis suggested to represent opposite points on a disease continuum.2

ACUTE PANCREATITIS

Risk Factors

No age, sex, or breed predisposition has been recognized in cats with acute pancreatitis, and no relationship has been established with body condition score.3-5

  • Cats over a wide age range, from kittens to geriatric cats, are affected; cats older than 7 years predominate.
  • In most cases, an underlying cause or instigating event cannot be determined, leading to classification as idiopathic.3
  • Abdominal trauma, sometimes from high-rise syndrome, is an uncommon cause that is readily identified from the history.6
  • The pancreas is sensitive to hypotension and ischemia; every effort must be taken to avoid hypotensive episodes under anesthesia.

Comorbidities
In cats with acute pancreatitis, the frequency of concurrent diseases is as high as 83% (Table 1).2

  • Pancreatitis complicates the management of some diabetic cats and may induce, for example, diabetic ketoacidosis.7
  • Anorexia attributable to pancreatitis can be the precipitating cause of hepatic lipidosis.8
  • The role of intercurrent inflammation in the biliary tract or intestine (also called triaditis) in the pathogenesis of pancreatitis is still uncertain.

Role of Bacteria

In one study, culture-independent methods to identify bacteria in sections of the pancreas from cats with pancreatitis detected bacteria in 35% of cases.9 This report renewed speculation about the role of bacteria in the pathogenesis of acute pancreatitis, and the potential role that the common insertion of the pancreatic duct and common bile duct into the duodenal papilla may play in facilitating reflux of enteric bacteria into the “common channel” in cats. Awareness of triaditis may affect the diagnostic evaluation of individual patients.

TABLE 1
Clinical Data from 95 Cats with Acute Pancreatitis (1976—1998; 59% Mortality Rate) & 89 Cats Diagnosed with Acute Pancreatitis (2004—2011; 16% Mortality Rate)
Number of Cats 95 89 75
50% 23% 18%
68% 41% 36%
25% 30% 32%
NA 12% 11%
NA 69% 68%
92% 37% 42%
NA 8% 5%
NA 11% 12%
7% 26% 11%
NA 21% 18%
NA 20% 19%
64% 45% 53%
64% 6% 6%
35%—52% 35% 36%
ALP = alkaline phosphatase; ALT = alanine aminotransferase; GGT = gamma glutamyl transferase; NA = not available
* Summarized from 4 published case series; a total of 56 cats had acute pancreatitis diagnosed at necropsy and 3 by pancreatic biopsy5,8,10,11
† Data obtained from reference12
‡ 68% of cats were hypothermic

High-rise syndrome

describes the phenomenon of cats falling from higher than 2 stories (23–30 feet); it also refers to injuries sustained during a fall.

DIAGNOSTIC EVALUATION

Many cats with pancreatitis have vague, nonspecific clinical signs, which make diagnosis challenging.5 Clinical signs related to common comorbidities, such as anorexia, lethargy, and vomiting, may overlap with, or initially mask, the signs associated with pancreatic disease.

Early publications on the clinical characteristics of acute pancreatitis required necropsy as an inclusion criterion, presumably skewing the spectrum of severity of the reported cases.5,8,10,11 Cats with chronic pancreatitis were excluded from these reports.

Clinical Findings

Table 1 lists common clinical findings in cats from necropsy-based reports and a recent series of 89 cats with acute pancreatitis studied by the authors.12

  • Note the lower prevalence of most clinical findings in the cats diagnosed clinically rather than from necropsy records.
  • In our evaluation of affected cats, 17% exhibited no signs aside from lethargy and 62% were anorexic.
  • Vomiting occurs inconsistently (35%—52% of cats).
  • Abdominal pain is detected in a minority of cases even when the index of suspicion of pancreatitis is high.
  • About ¼ of cats with pancreatitis have a palpable abdominal mass that may be misdiagnosed as a lesion of another intra-abdominal structure.

Laboratory Analyses

Hematologic abnormalities in cats with acute pancreatitis are nonspecific; findings may include nonregenerative anemia, hemoconcentration, leukocytosis, or leukopenia.

Serum biochemical profile results vary (Table 1). In our acute pancreatitis case series, 33% of cats had no abnormalities in their chemistry results at presentation.12

Serum cholesterol concentrations may be high in up to 72% of cases. Some cases of acute pancreatitis are associated with severe clinical syndromes, such as shock, disseminated intravascular coagulation, and multiorgan failure, that influence some serum parameters, such as albumin, liver enzymes, and coagulation tests.

Plasma ionized calcium concentrationmay be low, and has been correlated with a poorer outcome.11

Serum amylase activity is of no clinical value in the clinical diagnosis of pancreatitis in cats; it actually decreases in experimental feline pancreatitis.13 However, the serum activity of both amylase and lipase may increase whenever glomerular filtration rate is reduced.

Serum lipase activity is modestly increased early in experimentally induced disease, but is frequently normal in cats with spontaneous pancreatitis. A recent study found a high level of agreement between the 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester lipase assay and feline pancreas-specific lipase assay, suggesting that the method used for lipase measurement may influence sensitivity and specificity.14

Serum pancreatic lipase (Spec fPL, idexx.com) is the serum test that provides the most useful information to support, or exclude, a diagnosis of pancreatitis (see Feline Pancreatic Lipase Assays).

Feline Pancreatic Lipase Assays

The Spec fPL assay (idexx.com) is a commercially available monoclonal enzyme-linked immunosorbent assay. A study presented in abstract form estimated the sensitivity and specificity of this test for diagnosing feline pancreatitis at 79% and 82%, respectively.15

Concentration results are considered:

  • Diagnostic (positive) if ≥ 5.4 mcg/L
  • A gray zone if > 3.5 mcg/L and < 5.4 mcg/L
  • Negative if ≤ 3.5 mcg/L.

The Snap fPL (idexx.com) is a semiquantitative point-of-care test that can help rule out pancreatitis. A value of > 3.5 mcg/L is considered positive; therefore, a positive result must be confirmed by a Spec fPL assay.

With both tests, positive results must be interpreted in light of other clinical information, rather than considered an endpoint of diagnostic evaluation. After an episode of pancreatitis, the duration of fPL increase has not been reported.

Asymptomatic cats with persistently increased fPL concentrations may be encountered, especially if the fPL is included as a routine test in geriatric health panels. This may correlate with histologic evidence of pancreatitis reported in cats lacking clinical signs of disease.1

Abdominal Radiography
Exclusion of other causes of vague gastrointestinal signs, such as partial intestinal obstruction, is a major rationale for survey abdominal radiography in cats with clinical signs compatible with pancreatitis. Thoracic radiographs may detect pleural fluid or pulmonary edema, both of which have been associated with acute pancreatitis and other complications, such as pneumonia.

TABLE 2
Important Ultrasound Findings in Cats with Pancreatitis14,16-17
  • Increased echogenicity of mesenteric fat immediatel surrounding the pancreas*
  • Increased pancreatic thickness (enlarged pancreas)
  • Irregular pancreatic margins
  • Peripancreatic free fluid
  • Hypoechoic, hyperechoic, or mixed-echoic pancreas
  • Mass effect in cranial abdomen
  • Dilated common bile duct
* Abnormality with highest sensitivity, based on recent study16

 

Abdominal Ultrasonography

Abdominal ultrasonography is a key diagnostic test in cats suspected of having pancreatitis; Table 2 lists the most important ultrasound findings.

The reported sensitivity of abdominal ultrasound for detecting feline pancreatitis varies widely (11%— 68%),16 even when performed by board-certified radiologists. Therefore, some cats with biopsy-confirmed acute pancreatitis have no detectable sonographic abnormalities. However, the sensitivity of ultrasonography increases with increasing severity of pancreatitis.18

Abnormal sonographic findings are highly specific for pancreatitis—a cat with compatible clinical signs and visible changes in the pancreas is very likely to be correctly diagnosed with pancreatitis (Figure 2).

Fel Acute Pancr Fig 2

FIGURE 2. Sagital sonographic image of the left limb of the pancreas in an 8-year-old neutered male Maine Coon cat. The cat presented with diabetic ketoacidosis (new diagnosis), evidence of abdominal pain, and a palpable midcranial abdominal mass. The pancreas is enlarged and hypoechoic (up arrow) with irregular margins. The mesentery adjacent to the pancreas (horizontal arrow) is hyperechoic (reactive). These changes are consistent with pancreatitis. Courtesy Dr. Kari Anderson, University of Minnesota Veterinary Medical Center

Fine-Needle Aspiration

Ultrasound-guided fine-needle aspirates of the pancreas and/or peripancreatic tissue may assist in the diagnosis of pancreatitis (Figure 3), and may also be helpful when nodular changes are present.4,12

Fel Acute Pancr Fig 3

FIGURE 3. Pancreatic aspirate from a cat with pancreatitis (200×, Wright’s-Giemsa stain). There are multiple cohesive clusters of slightly hyperplastic pancreatic exocrine cells characterized by increased cytoplasmic basophilia (horizontal arrow). The background contains blood and increased numbers of neutrophils (vertical arrow) with occasional foamy macrophages. Courtesy of Dr. Leslie Sharkey, University of Minnesota Veterinary Medical Center

INITIAL THERAPY

The initial medical management of cats with acute pancreatitis must not be delayed until a diagnosis is confirmed. In experimental studies, a major factor in the progression of mild pancreatitis to severe pancreatitis is disturbed pancreatic microcirculation.

Early IV fluid therapy with a balanced, isotonic replacement crystalloid (eg, lactated Ringer’s solution, 0.9% saline, Plasma-Lyte 156, Normosol-R), supplemented with potassium and glucose as necessary, is recommended. This emphasis on early fluid resuscitation is consistent with human treatment guidelines for acute pancreatitis and is of critical importance.19

Potassium supplementation (up to 20—30 mEq potassium chloride/L of fluids) is necessary to replace losses and address reduced intake, and should be monitored by serial measurement of serum potassium levels. The level of supplementation may need to be reduced in patients with mild clinical signs, or increased in patients with concurrent diabetic ketoacidosis.

Calcium gluconate (50—150 mg/kg IV as a slow bolus) may be required for symptomatic hypocalcemia (tremors, seizure activity), a possible complication of acute pancreatitis, and serum ionized calcium concentrations should be monitored regularly during calcium therapy. Begin with a portion of this dose, and discontinue if ionized calcium normalizes. Continuous low-dose IV infusions of calcium gluconate (5—10 mg/kg/H IV) are required by some cats.

Insulin therapy is initiated in diabetic patients.5

Colloids, such as hydroxyethyl starch, are useful when hypoproteinemia is present, and may have antithrombotic effects that help maintain microcirculation. However, use of synthetic colloids in companion animals is increasingly being debated due to adverse effects on renal function noted in human patients.20

Plasma transfusion theoretically provides a source of circulating protease inhibitors, but numerous human studies fail to support its use, and 1 retrospective canine pancreatitis study failed to demonstrate a benefit.

Learn More

Read Treatment Guidelines for Acute Pancreatitis in Cats for indepth information on therapeutic approaches, medications, and dosages.

MEDICAL THERAPY

Antiemetics

Nausea and vomiting may be severe in patients with acute pancreatitis.

  • The potent antiemetic maropitant, an NK1 receptor antagonist, is useful for controlling emesis (and probably nausea) and providing visceral analgesia.21
  • An alternative antiemetic is a 5-HT3 antagonist (ondansetron or dolasetron), which may be combined with maropitant in severe cases.
  • The dopaminergic antagonist metoclopramide may help enhance motility in the upper gastrointestinal tract. It acts as a weak peripherally acting antiemetic in dogs, but this effect is questionable in cats.
  • The histamine-2 receptor antagonist ranitidine may be selected for dual acid inhibition and prokinetic effects. Correction of hypokalemia also helps improve gastrointestinal motility.

Gastroprotectants

Gastric acid suppression is commonly incorporated into therapy for feline acute pancreatitis. The rationale includes protecting:

  • The esophagus from exposure to gastric acid during episodes of vomiting
  • Against gastric ulceration, to which patients with pancreatitis may be predisposed due to hypovolemia and local peritonitis.

Higher gastric pH may decrease exocrine pancreatic stimulation but remains undocumented as a treatment for pancreatitis.

When gastric acid suppression is desired, a proton-pump inhibitor (pantoprazole) may be preferred over a histamine-2 receptor antagonist; an experimental study in rats demonstrated that pantoprazole reduced inflammatory changes and leakage of pancreatic acinar cells.22

When a histamine-2 receptor antagonist is used, famotidine is believed to be most effective for suppression of gastric acid production.

Analgesics

Pain management is a critical aspect of treating acute pancreatitis, and can be easily overlooked because cats may not exhibit easily recognized signs of pain. Analgesia can be provided using opioids, such as buprenorphine or fentanyl, delivered by IV or SC injection, sublingual route, or transdermal patch.

Convincing evidence suggests that the antiemetic maropitant also provides visceral analgesia.21 Tramadol is usually avoided in cats because it can cause severe dysphoria.

Antibiotics

Acute pancreatitis is thought to begin as a sterile process, and reports of bacterial complications, such as pancreatic abscessation, are uncommon. Broad-spectrum antibiotics may be warranted in cats with complete blood count findings suggestive of sepsis but, otherwise, are not routinely used.

However, a recent study in cats using culture-independent methods9 suggested that bacterial infection may warrant greater consideration. Coliforms are the principal pathogens, and are also seen in bile cultures from cats with cholangitis.23

Glucocorticoids

Historical reluctance to use corticosteroids for treating pancreatitis has been based on concern that these agents could lead to pancreatitis; however, no evidence supports this assumption in cats.

Corticosteroids exert broad anti-inflammatory effects, and may have a role in increasing production of pancreatitis-associated protein, which helps protect against inflammation. They may also address critical illness-related corticosteroid insufficiency, a relative adrenal insufficiency that could occur in acute pancreatitis.

Steroid use in cats with acute pancreatitis is being reconsidered but remains unexamined. There is no existing data supporting the use of corticosteroids in feline pancreatitis, and care must be exercised when considering their use in cats with diabetes. Judicious short-term corticosteroid administration may be considered in a cat with severe acute pancreatitis that is failing to respond to other therapies.

NUTRITIONAL THERAPY

In cats suspected of having acute pancreatitis, oral intake has historically been initially withheld for 24 to 48 H; then gradually re-introduced, as tolerated. The theory behind this rationale—which has come under close scrutiny in human and veterinary medicine—was to “rest” the pancreas by decreasing pancreatic stimulation.

Clinical and experimental data support the concept that nutritional management plays an important therapeutic role in recovery from acute pancreatitis. The current standard of care—which attempts to maintain enterocyte integrity, reduce risk for bacterial translocation, and attenuate the systemic inflammatory response—is to:24,25

  • Administer antiemetics immediately upon presentation; then as required to control vomiting
  • Begin enteral feeding as soon as possible
  • Only implement parenteral nutrition in patients in which refractory vomiting precludes enteral support (rare). A small prospective controlled study in dogs with acute pancreatitis demonstrated that the group fed via esophagostomy tube had significantly fewer episodes of vomiting or regurgitation compared with the group fed parenterally.26

A nasoesophageal tube or esophagostomy tube may be used to provide nutritional support to cats with acute pancreatitis; this also helps treat or prevent concurrent hepatic lipidosis. A liquid diet must be fed through a nasoesophageal tube (see Treatment Guidelines for Acute Pancreatitis in Cats); a variety of diets will pass through an esophagostomy tube. The volume of food fed is increased toward calculated resting energy requirement as tolerance permits.

SURGICAL THERAPY

Exploratory laparotomy (or laparoscopy) to obtain pancreatic biopsy specimens in a cat suspected of having acute pancreatitis is not indicated, but pancreatic biopsy can be performed with relative safety if the abdomen is being explored for other reasons.27

Surgery is rarely needed to remove devitalized or infected tissue. Serum bilirubin may remain increased for weeks during apparent recovery from a bout of pancreatitis, but surgery is only occasionally required to relieve an obstruction of the common bile duct.28 Fluid accumulation within the pancreas usually resolves spontaneously.

fPL = feline pancreatic lipase

References

  1. De Cock HE, Forman MA, Farver TB, et al. Prevalence and histopathologic characteristics of pancreatitis in cats. Vet Pathol 2007; 44:39-49.
  2. Ferrari JA, Hardam E, Kimmel SE, et al. Clinical differentiation of acute necrotizing from chronic nonsuppurative pancreatitis in cats: 63 cases (1996-2001). JAVMA 2002; 223:469-474.
  3. Bazelle J, Watson P. Pancreatitis in cats: Is it acute, is it chronic, is it significant? J Fel Med Surg2014; 16:395-406.
  4. Armstrong PJ, Williams DA. Pancreatitis in cats. Top Companion Anim Med 2012; 27:140-147.
  5. Hill RC, Van Winkle TJ. Acute necrotizing pancreatitis and acute suppurative pancreatitis in the cat. A retrospective study of 40 cases (1976—1989). J Vet Intern Med 1993; 7:25-33.
  6. Zimmermann E, Hittmair KM, Suchodolski JS, et al. Serum feline-specific pancreatic lipase immunoreactivity concentrations and abdominal ultrasonographic findings in cats with trauma resulting from high-rise syndrome. JAVMA 2013; 242:1238-1243.
  7. Caney SMA. Pancreatitis and diabetes in cats. Vet Clin Small Anim Pract 2013; 43:303-317.
  8. Akol KG, Washabau RW, Saunders HM, Hendrick MJ. Acute pancreatitis in cats with hepatic lipidosis.J Vet Intern Med 1993; 7:205-209.
  9. Simpson KW, Twedt DC, McDonough SP, et al. Culture-independent detection of bacteria in feline pancreatitis. ACVIM Forum Proc, 2011.
  10. Simpson KW, Shiroma JT, Biller DS, et al. Ante mortem diagnosis of pancreatitis in four cats. J Small Anim Pract 1994; 35:93-99.
  11. Kimmel SE, Washabau RJ, Drobatz KJ. Incidence and prognostic value of low plasma ionized calcium concentration in cats with acute pancreatitis: 46 cases (1996-1998). JAVMA 2001; 219:1105-1109.
  12. Crain SK, Sharkey LC, Cordner AP, et al. Safety of ultrasound-guided fine-needle aspiration of the feline pancreas: A case-control study. J Feline Med Surg 2014 (epub ahead of print).
  13. Kitchell BE, Strombeck DR, Cullen J, Harrold D. Clinical and pathologic changes in experimentally induced acute pancreatitis in cats. Am J Vet Res 1986; 47:1170-1173.
  14. Oppliger S, Hartnack S, Riond B, et al. Agreement of the serum Spec fPLTM and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester lipase assay for the determination of serum lipase in cats with suspicion of pancreatitis. J Vet Intern Med 2013; 27:1077-1082.
  15. Forman MA, Shiroma J, Armstrong PJ, et al. Evaluation of feline pancreas-specific lipase (Spec fPL®) for the diagnosis of feline pancreatitis (ACVIM abstract 165). J Vet Intern Med 2009; 23:733-734.
  16. Williams JM, Panciera DL, Larson MM, Were SR. Ultrasonographic findings in cats with elevated serum pancreatic lipase immunoreactivity. J Vet Intern Med 2013; 27:913-918.
  17. Hecht S, Henry G. Sonographic evaluation of the normal and abnormal pancreas. Clin Tech Small Anim Pract 2007; 22:115-121.
  18. Forman MA, Marks SL, De Cock HE, et al. Evaluation of serum feline pancreatic lipase immunoreactivity and helical computed tomography versus conventional testing for the diagnosis of feline pancreatitis. J Vet Intern Med 2004; 18:807-815.
  19. Wu BU, Conwell DL. Acute pancreatitis Part 1: Approach to early management. Clin Gastroent Hepatol 2010; 8:410-415.
  20. Glover PA, Rudloff E, Kirby R. Hydroxyethyl starch: A review of pharmacokinetics, pharmacodynamics, current products, and potential clinical risks, benefits, and use. J Vet Emer Crit Care 2014; 24(6):642-661.
  21. Niyom S, Boscan P, Twedt DC, et al. Effect of maropitant, a neurokinin-1 receptor antagonist, on the minimum alveolar concentration of sevoflurane during stimulation of the ovarian ligament in cats. Vet Anaesth Analg 2013; 40:425-431.
  22. Hackert T, Tudor S, Felix K, et al. Effects of pantoprazole in experimental acute pancreatitis. Life Sci 2010; 87:551-557.
  23. Twedt DC, Armstrong PJ, Simpson KW. Feline cholangitis. In Bonagura JD, Twedt DC (eds): Current Veterinary Therapy XV, Small Animal Practice. St Louis: Elsevier Saunders, 2014, pp 614-619.
  24. Jenson KB, Chan DL. Nutritional management of acute pancreatitis in dogs and cats. J Vet Emerg Crit Care 2014; 24:240-250.
  25. Klaus J, Rudloff E, Kirby R. Nasogastric tube feeding in cats with suspected acute pancreatitis: 55 cases (2001-2006). J Vet Emerg Crit Care 2009; 19:337-346.
  26. Mansfield CS, James FE, Steiner JM, et al. A pilot study to assess tolerability of early enteral nutrition via esophagostomy tube feeding in dogs with severe acute pancreatitis. J Vet Intern Med 2011; 25:419-425.
  27. Pratschke KM, Ryan J, McAlinden A, McLauchlan G. Pancreatic surgical biopsy in 24 dogs and 19 cats: Postoperative complications and clinical relevance of histological findings. J Small Anim Pract 2014 (epub ahead of print).
  28. Son TT, Thompson L, Serrano SLV, Seshadri R. Surgical intervention in the management of severe acute pancreatitis in cats: 8 cases (2003-2007). J Vet Emer Crit Care 2010; 20:426-435.

P. Jane ArmstrongP. Jane Armstrong, DVM, MS, MBA, Diplomate ACVIM, is a professor in the Veterinary Clinical Sciences Department at University of Minnesota. She is past president of the Comparative Gastroenterology Society and Small Animal Internal Medicine of ACVIM, and serves on the Editorial Advisory Board for TVP. She is widely published and has lectured around the world. She received her DVM from Ontario Veterinary College (Guelph, Canada), and completed an internship at University of Illinois and residency at Michigan State University.

 

Sarah CrainSarah Crain, DVM, MS, Diplomate ACVIM, is currently in a PhD program at Cummings School of Veterinary Medicine at Tufts University, exploring the utility and mechanism of stem cell therapies for canine inflammatory diseases. Dr. Crain received her DVM at University of Minnesota, where she also completed a residency in small animal internal medicine following an internship at North Carolina State University. Dr. Crain’s primary professional interests are gastrointestinal disease and auto-immune/hematologic diseases.

 

 


P. Jane Armstrong, DVM, MS, MBA, Diplomate ACVIM, University of Minnesota, and Sarah Crain, DVM, MS, Diplomate ACVIM, Tufts University

Chronic pancreatitis appears to be much more common in cats than acute pancreatitis (Figure 1).1-4 Unfortunately, there is poor correlation between the usual clinical definition of chronic (time course) and histologic definition of chronic (fibrosis, lymphocytic inflammation, and acinar atrophy) (Figure 2). Adding to the complexity of feline chronic pancreatitis is evidence that it can be very mild or asymptomatic and has a high histologic prevalence in apparently healthy cats.1

Fel Acute In Brief Fig 1

FIGURE 1. Duodenum (D) and duodenal limb of the pancreas (P) in a cat with chronic pancreatitis and nodular regeneration of the exocrine pancreas; the entire parenchyma is composed of regenerative nodules.

FIGURE 2. Histomicrograph of the pancreas (P) with chronic fibrosing lymphoplasmacytic pancreatitis and nodular regeneration; the parenchyma is dissected by strands of fibrous tissue infiltrated by lymphocytes and plasma cells (arrows). Hematoxylin and eosin stain, 20× magnification.

FIGURE 2. Histomicrograph of the pancreas (P) with chronic fibrosing lymphoplasmacytic pancreatitis and nodular regeneration; the parenchyma is dissected by strands of fibrous tissue infiltrated by lymphocytes and plasma cells (arrows). Hematoxylin and eosin stain, 20× magnification.

DIAGNOSTIC EVALUATION

Histologic features of acute and chronic pancreatitis overlap somewhat, suggesting that they may represent different points on a disease spectrum.

In the Literature

One necropsy-based study of 63 cats could not identify clinical features helpful in distinguishing acute from chronic pancreatitis.5

  • Notably, abdominal ultrasonography results were unremarkable in 50% of all cats; when pancreatic abnormalities were detected, findings did not differ between cats with acute and those with chronic pancreatitis.
  • Concurrent disease was common in both groups of cats, but 100% of cats with chronic pancreatitis had one or more concurrent diseases (Table).

Ultrasonography Findings

Ultrasonographic findings in cats with histologically confirmed chronic pancreatitis overlap considerably with findings in cats with acute pancreatitis (Table).5,6 Given the clinical and histologic overlap between these forms of the disease, this is not surprising.

Fine-Needle Aspiration

Nodular changes may develop; fine-needle aspiration cytology may provide a useful minimally invasive method of investigation.3,7

Treatment Guidelines

See Treatment Guidelines for Acute Pancreatitis for dosages of mirtazapine, maropitant, and SAMe.

THERAPEUTIC MEASURES

Nutritional Therapy

There is no evidence that a low-fat diet helps treat or prevent pancreatitis in cats. The authors’ choice is to feed cats with a history of pancreatitis a diet high in antioxidants and provide S-adenosyl methionine (SAMe) as an antioxidant supplement. A highly digestible diet with a novel or hydrolyzed protein source may be of benefit if concurrent inflammatory bowel disease is present.

Medical Therapy

Anti-inflammatory doses of prednisolone (2.5—5 mg/cat Q 48—72 H) are increasingly being used in cats with presumed chronic (or intermittent relapsing) pancreatitis, along with:

  • Mirtazapine on an ongoing basis as needed for appetite stimulation (mirtazapine appears to have an antiemetic effect as well)
  • Maropitant at the first indication of relapse (declining appetite, apparent nausea, or vomiting).

Coexisting conditions, such as cholangitis and inflammatory bowel disease, are common in cats with pancreatitis and often must be managed concurrently. No evidence suggests that steroid use is problematic in cats with chronic pancreatitis.

Exocrine Pancreatic Insufficiency

Exocrine pancreatic insufficiency is more common in cats than previously believed, and most cases are due to chronic pancreatitis.8Measurement of serum trypsin-like immunoreactivity (TLI) is recommended in cats with weight loss, loose stools, and/or polyphagia. Some cats have greasy soiling of the hair in the perianal region, and most cats with exocrine pancreatic insufficiency have a severely decreased serum cobalamin concentration, which can lead to various gastrointestinal and systemic complications and to treatment failure.Pancreatic enzyme supplements are used in some humans with chronic pancreatitis with normal exocrine pancreatic function because they are associated with decreased frequency and intensity of episodes of abdominal pain.2,3 This has not been investigated in cats, but there are anecdotal reports that this therapy improves appetite and gastrointestinal signs in cats with chronic pancreatitis.2

SAMe = S-adenosyl methionine; TLI = trypsin-like immunoreactivity

References

  1. De Cock HE, Forman MA, Farver TB, et al. Prevalence and histopathologic characteristics of pancreatitis in cats. Vet Pathol 2007; 44:39-49.
  2. Bazelle J, Watson P. Pancreatitis in cats: Is it acute, is it chronic, is it significant? J Fel Med Surg 2014; 16:395-406.
  3. Armstrong PJ, Williams DA. Pancreatitis in cats. Top Companion Anim Med 2012; 27:140-147.
  4. Xenoulis PG, Suchodolski JS, Steiner JM. Chronic pancreatitis in dogs and cats. Compend Contin Educ Pract Vet 2008; 30:166-180.
  5. Ferrari JA, Hardam E, Kimmel SE, et al. Clinical differentiation of acute necrotizing from chronic nonsuppurative pancreatitis in cats: 63 cases (1996-2001). JAVMA 2002; 223:469-474.
  6. Oppliger S, Hartnack S, Reusch CE, Kook PH. Agreement of serum feline pancreas-specific lipase and colorimetric lipase assays with pancreatic ultrasonographic findings in cats with suspicion of pancreatitis: 161 cases (2008-2012). JAVMA 2014; 244:1060-1065.
  7. Crain SK, Sharkey LC, Cordner AP, et al. Safety of ultrasound-guided fine-needle aspiration of the feline pancreas: A case-control study. J Feline Med Surg 2014 (epub ahead of print).
  8. Steiner JM. Exocrine pancreatic insufficiency in the cat. Top Companion Anim Med 2012; 27:113-116.

 

Treatment Guidelines for Acute Pancreatitis in Cats

P. Jane Armstrong, DVM, MS, MBA, Diplomate ACVIM, University of Minnesota
Sarah Crain, DVM, MS, Diplomate ACVIM, Tufts University
Read Feline Acute Pancreatitis: Current Concepts in Diagnosis & Therapy for further details.

Balanced isotonic replacement crystalloid Maintenance at 40—60 mL/kg Q 24 H
Additional replacement of ongoing losses may be required
Rehydrate according to speed of losses, monitor weight and urine production, and account for cardiovascular disease
Potassium chloride 20—30 mEq/L to start; adjust depending on:
  • Serum potassium values
  • Fluid rate
As indicated by potassium deficit:
  • Replace total body losses resulting from vomiting or anorexia, or if managing diabetes
  • Reduce in less symptomatic patients
Calcium gluconate 50—150 mg/kg IV bolus (if symptomatic for hypocalcemia)
5-—10 mg/kg/H IV CRI (if needed)
With serial monitoring, discontinue when patient normalizes
Maropitant 1 mg/kg SC, PO, or IV Q 24 H Refrigerate to reduce pain associated with SC injection
IV use is extralabel
Provides visceral analgesia
Ondansetron 0.5—1 mg/kg IV Q 12 H or 24 H Administer IV injection slowly
Dolasetron 0.5—1 mg/kg PO or SC Q 12 H or 24 H
Metoclopramide 0.2—0.4 mg/kg SC or PO Q 6—8 H
1—2 mg/kg IV/day CRI Q 24 H
Watch for drug interactions
May induce neurologic signs
Ineffective antiemetic in cats
Pantoprazole 1 mg/kg IV Q 24 H
Omeprazole 0.7—1 mg/kg PO Q 24 H May reduce absorption of other medications
Famotidine 0.5—1 mg/kg IV or PO Q 12 H or 24 H Administer IV injection slowly to avoid hypotension
Reports of intravascular hemolysis when IV used in cats
Ranitidine 1—2 mg/kg IV or PO Q 12 H Mild prokinetic effect
Administer IV injection slowly to avoid hypotension
Buprenorphine 0.005—0.02 mg/kg SC, IV, or sublingual Q 6—8 H Adverse effects uncommon
Can produce sedation
Fentanyl Loading dose of 1—4 mcg/kg; then 1—4 mcg/kg/H IV CRI per H Do not combine with buprenorphine or butorphanol
Fentanyl patch 12.5 mcg per H patch or 25 mcg per H patch Patch lasts 3—4 days once applied
Effect noted in 6—12 H
May cover half of 25-mcg patch if needed
Butorphanol 0.1—0.2 mg/kg per H IV CRI, after loading dose of 0.1—0.2 mg/kg IV 0.2—0.4 mg/kg SC, IM, or IV May not provide sufficient analgesia when used alone; often combined with ketamine (loading dose, 0.1 mg/kg IV; IV CRI, 0.4 mg/kg/H)
Intermittent administration only may provide analgesia for 1 H or less
Ampicillin
Amoxicillin
10—20 mg/kg IV or SC Q 8 H
10—20 mg/kg PO Q 12 H
Useful in combination with metronidazole
Ampicillin has poor bioavailability when administered orally
Ampicillin/amoxicillin with sulbactam 20—30 mg/kg IV Q 8 H
62.5 mg/cat PO Q 12 H
Sulbactam may cause diarrhea/inappetence
Enrofloxacin 5 mg/kg IV or PO Q 24 H Useful in combination with metronidazole
Marbofloxacin 2.5—5 mg/kg PO Q 24 H Useful in combination with metronidazole
Metronidazole 10—15 mg/kg IV or PO Q 12 H Not suitable for use alone
Best in combination with aerobic/gram-positive targeting therapy
Nutrition
Clinicare Canine/ Feline Liquid Diet or Vivonex (1 kcal/mL)
Via nasoesophageal tube as:
  • Continuous infusion
  • Multiple small bolus feedings
Achieve RER over 3—5 days:
      • Body

weight (kg)0.75

    • × 70

Reduced-fat diet not indicated in cats

Mirtazapine
(appetite stimulant)
1.88—3.75 mg/cat PO Q 2—3 days Also has antiemetic effect
Main side effect is increased affection
Sedation is dose-related
Do not administer with tramadol
Regular insulin Based on blood glucose monitoring:
0.1—0.2 U/kg SC or IM Q 4 H
1.1 U/kg per day IV CRI, with or without dextrose supplementation
For patients with diabetic ketoacidosis or inappetent diabetic patients
Strict monitoring of blood glucose required
Pancreatitis may destabilize a previously controlled diabetic patient
S-adenosyl methionine (SAMe) Cats < 5 kg: 90 mg PO Q 24 H
Cats > 5 kg: 180 mg or 225 mg PO Q 24 H
Give intact tablet on an empty stomach; may be useful with concurrent liver disease
Cyanocobalamin
(Vitamin B12)
250 mcg/cat SC weekly for 6 weeks, then 30 days later; retest after 30 days Empirical use or based on serum concentration
May be useful in cats with concurrent IBD or hepatic lipidosis
B vitamin complex 1—2 mL/L of IV fluids May be useful in cats with prolonged anorexia
Vitamin K1 0.5—1.5 mg/kg SC Q 12 H May be useful in hyperbilirubinemic patients (ie, concurrent hepatic lipidosis)
Use 25-gauge needle; avoid IV use due to risk of anaphylaxis
CRI = constant-rate infusion; IBD = inflammatory bowel disease; RER = resting energy requirement

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