{"id":6,"date":"2015-02-23T01:03:44","date_gmt":"2015-02-23T01:03:44","guid":{"rendered":"http:\/\/phosdev.com\/todaysveterinarypractice\/?p=6"},"modified":"2022-10-25T19:48:02","modified_gmt":"2022-10-25T19:48:02","slug":"current-issue-feline-acute-pancreatitis","status":"publish","type":"post","link":"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/hepatology\/current-issue-feline-acute-pancreatitis\/","title":{"rendered":"Feline Acute Pancreatitis: Current Concepts in Diagnosis and Therapy"},"content":{"rendered":"<p>Pancreatitis appears to be a common disease in cats,<sup>1<\/sup> 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.<\/p>\n<h2>Profile<\/h2>\n<h3>Acute Versus Chronic Pancreatitis<\/h3>\n<p><em>Acute pancreatitis<\/em> is characterized by neutrophilic inflammation, with variable amounts of pancreatic acinar cell and peripancreatic fat necrosis (<strong>Figure 1<\/strong>).<sup>1<\/sup> Evidence is mounting that chronic pancreatitis (see <strong>In Brief: Diagnosis &amp; Treatment of Feline Chronic Pancreatitis<\/strong>) is more common than the acute form, but sonographic and other clinical findings overlap considerably between the 2 forms of disease.<sup>1-3<\/sup><\/p>\n<div id=\"attachment_8125\" style=\"width: 310px\" class=\"wp-caption aligncenter\"><a href=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2015\/02\/Fel-Acute-Pancr-Fig-1.png\"><img fetchpriority=\"high\" decoding=\"async\" aria-describedby=\"caption-attachment-8125\" class=\"wp-image-8125 size-full\" src=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2015\/02\/Fel-Acute-Pancr-Fig-1.png\" alt=\"Fel Acute Pancr Fig 1\" width=\"300\" height=\"256\" \/><\/a><p id=\"caption-attachment-8125\" class=\"wp-caption-text\">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). <em>Courtesy Dr. Arno Wuenschmann, Minnesota Veterinary Diagnostic Laboratory<\/em><\/p><\/div>\n<h3>Diagnostic Challenges<\/h3>\n<p>Use of histopathology as the gold standard for diagnosis has recently been questioned because of the potential for histologic ambiguity.<sup>3,4<\/sup> 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.<sup>1<\/sup> 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.<\/p>\n<h3>Prevalence<\/h3>\n<p>Such considerations help explain the wide range in the reported prevalence of feline pancreatitis, from 0.6% to 67%.<sup>3<\/sup> 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.<sup>2<\/sup><\/p>\n<h2>Acute Pancreatitis<\/h2>\n<h3>Risk Factors<\/h3>\n<p>No age, sex, or breed predisposition has been recognized in cats with acute pancreatitis, and no relationship has been established with body condition score.<sup>3-5<\/sup><\/p>\n<ul>\n<li>Cats over a wide age range, from kittens to geriatric cats, are affected; cats older than 7 years predominate.<\/li>\n<li>In most cases, an underlying cause or instigating event cannot be determined, leading to classification as <em>idiopathic<\/em>.<sup>3<\/sup><\/li>\n<li>Abdominal trauma, sometimes from <em>high-rise syndrome<\/em>, is an uncommon cause that is readily identified from the history.<sup>6<\/sup><\/li>\n<li>The pancreas is sensitive to hypotension and ischemia; every effort must be taken to avoid hypotensive episodes under anesthesia.<\/li>\n<\/ul>\n<p><strong class=\"TVPGray\">Comorbidities<\/strong><br \/>\nIn cats with acute pancreatitis, the frequency of concurrent diseases is as high as 83% (<strong>Table 1<\/strong>).<sup>2<\/sup><\/p>\n<ul>\n<li>Pancreatitis complicates the management of some diabetic cats and may induce, for example, diabetic ketoacidosis.<sup>7<\/sup><\/li>\n<li>Anorexia attributable to pancreatitis can be the precipitating cause of hepatic lipidosis.<sup>8<\/sup><\/li>\n<li>The role of intercurrent inflammation in the biliary tract or intestine (also called triaditis) in the pathogenesis of pancreatitis is still uncertain.<\/li>\n<\/ul>\n<table border=\"0\" width=\"540\" cellpadding=\"5\">\n<tbody>\n<tr>\n<td colspan=\"4\"><span class=\"arial\">TABLE 1<br \/>\n<strong>Clinical Data from 95 Cats with Acute Pancreatitis (1976\u20131998; 59% Mortality Rate) &amp; 89 Cats Diagnosed with Acute Pancreatitis (2004\u20132011; 16% Mortality Rate)<\/strong><br \/>\n<\/span><\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\" bgcolor=\"#f5821f\">\n<td class=\"NAVCOrange2\"><strong>PARAMETER<\/strong><\/td>\n<td class=\"NAVCOrange2\"><strong>HISTORICAL DATA*<\/strong><\/td>\n<td class=\"NAVCOrange2\"><strong>CATS WITH PANCREATITIS\u2020<\/strong><\/td>\n<td class=\"NAVCOrange2\"><strong>SURVIVING CATS WITH PANCREATITIS\u2020<\/strong><\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\" bgcolor=\"#f9bc88\">\n<td><strong>Number of Cats<\/strong><\/td>\n<td><strong>95<\/strong><\/td>\n<td><strong>89<\/strong><\/td>\n<td><strong>75<\/strong><\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">ALP elevation<\/td>\n<td>50%<\/td>\n<td>23%<\/td>\n<td>18%<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">ALT elevation<\/td>\n<td>68%<\/td>\n<td>41%<\/td>\n<td>36%<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">Apparent abdominal pain<\/td>\n<td>25%<\/td>\n<td>30%<\/td>\n<td>32%<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">Cholangitis<\/td>\n<td>NA<\/td>\n<td>12%<\/td>\n<td>11%<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">Concurrent disease diagnosed<\/td>\n<td>NA<\/td>\n<td>69%<\/td>\n<td>68%<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">Dehydration<\/td>\n<td>92%<\/td>\n<td>37%<\/td>\n<td>42%<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">Diabetic ketoacidosis<\/td>\n<td>NA<\/td>\n<td>8%<\/td>\n<td>5%<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">Diabetes mellitus<\/td>\n<td>NA<\/td>\n<td>11%<\/td>\n<td>12%<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">Fever<\/td>\n<td>7%<sup>\u2021<\/sup><\/td>\n<td>26%<\/td>\n<td>11%<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">GGT elevation<\/td>\n<td>NA<\/td>\n<td>21%<\/td>\n<td>18%<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">Hepatic lipidosis<\/td>\n<td>NA<\/td>\n<td>20%<\/td>\n<td>19%<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">Hyperbilirubinemia<\/td>\n<td>64%<\/td>\n<td>45%<\/td>\n<td>53%<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">Icterus<\/td>\n<td>64%<\/td>\n<td>6%<\/td>\n<td>6%<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\">Vomiting<\/td>\n<td>35%\u201352%<\/td>\n<td>35%<\/td>\n<td>36%<\/td>\n<\/tr>\n<tr>\n<td class=\"references\" style=\"text-align: left\" colspan=\"4\">ALP = alkaline phosphatase; ALT = alanine aminotransferase; GGT = gamma glutamyl transferase; NA = not available<\/td>\n<\/tr>\n<tr>\n<td class=\"references\" style=\"text-align: left\" colspan=\"4\">* Summarized from 4 published case series; a total of 56 cats had acute pancreatitis diagnosed at necropsy and 3 by pancreatic biopsy<sup>5,8,10,11<\/sup><br \/>\n\u2020 Data obtained from reference<sup>12<\/sup><br \/>\n\u2021 68% of cats were hypothermic<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<h3><strong class=\"TVPGray\">Role of Bacteria<\/strong><\/h3>\n<p>In one study, culture-independent methods to identify bacteria in sections of the pancreas from cats with pancreatitis detected bacteria in 35% of cases.<sup>9<\/sup> 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 &#8220;common channel&#8221; in cats. Awareness of triaditis may affect the diagnostic evaluation of individual patients.<\/p>\n<h2>Diagnostic Evaluation<\/h2>\n<p>Many cats with pancreatitis have vague, nonspecific clinical signs, which make diagnosis challenging.<sup>5<\/sup> Clinical signs related to common comorbidities, such as anorexia, lethargy, and vomiting, may overlap with, or initially mask, the signs associated with pancreatic disease.<\/p>\n<p>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.<sup>5,8,10,11<\/sup> Cats with chronic pancreatitis were excluded from these reports.<\/p>\n<h3><strong class=\"TVPGray\">Clinical Findings<\/strong><\/h3>\n<p><strong>Table 1<\/strong> lists common clinical findings in cats from necropsy-based reports and a recent series of 89 cats with acute pancreatitis studied by the authors.<sup>12<\/sup><\/p>\n<ul>\n<li>Note the lower prevalence of most clinical findings in the cats diagnosed clinically rather than from necropsy records.<\/li>\n<li>In our evaluation of affected cats, 17% exhibited no signs aside from lethargy and 62% were anorexic.<\/li>\n<li>Vomiting occurs inconsistently (35%\u201352% of cats).<\/li>\n<li>Abdominal pain is detected in a minority of cases even when the index of suspicion of pancreatitis is high.<\/li>\n<li>About \u00bc of cats with pancreatitis have a palpable abdominal mass that may be misdiagnosed as a lesion of another intra-abdominal structure.<\/li>\n<\/ul>\n<h3><strong class=\"TVPGray\">Laboratory Analyses<\/strong><\/h3>\n<p><strong>Hematologic abnormalities<\/strong> in cats with acute pancreatitis are nonspecific; findings may include nonregenerative anemia, hemoconcentration, leukocytosis, or leukopenia.<\/p>\n<p><strong>Serum biochemical profile<\/strong> results vary (<strong>Table 1<\/strong>). In our acute pancreatitis case series, 33% of cats had no abnormalities in their chemistry results at presentation.<sup>12<\/sup><\/p>\n<p><strong>Serum cholesterol concentrations<\/strong> 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.<\/p>\n<p><strong>Plasma ionized calcium concentration<\/strong>may be low, and has been correlated with a poorer outcome.<sup>11<\/sup><\/p>\n<p><strong>Serum amylase activity<\/strong> is of no clinical value in the clinical diagnosis of pancreatitis in cats; it actually decreases in experimental feline pancreatitis.<sup>13 <\/sup>However, the serum activity of both amylase and lipase may increase whenever glomerular filtration rate is reduced.<\/p>\n<p><strong>Serum lipase activity<\/strong> 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&#8242;-methylresorufin) ester lipase assay and feline pancreas-specific lipase assay, suggesting that the method used for lipase measurement may influence sensitivity and specificity.<sup>14<\/sup><\/p>\n<p><strong>Serum pancreatic lipase<\/strong> (Spec fPL, idexx.com) is the serum test that provides the most useful information to support, or exclude, a diagnosis of pancreatitis (see <strong>Feline Pancreatic Lipase Assays<\/strong>).<\/p>\n<div class=\"orange-box\">\n<h3><span class=\"NAVCOrange2\">Feline Pancreatic Lipase Assays<\/span><\/h3>\n<p>The <strong><span class=\"NAVCOrange2\">Spec fPL assay<\/span><\/strong> (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.<sup><span style=\"font-size: small\">15<\/span><\/sup><\/p>\n<p>Concentration results are considered:<\/p>\n<ul>\n<li>Diagnostic (positive) if <strong class=\"NAVCOrange2\">\u2265 5.4 mcg\/L<\/strong><\/li>\n<li>A gray zone if <strong class=\"NAVCOrange2\">&gt; 3.5 mcg\/L and &lt; 5.4 mcg\/L<\/strong><\/li>\n<li>Negative if <span class=\"NAVCOrange2\"><strong>\u2264 3.5 mcg\/L<\/strong><\/span>.<\/li>\n<\/ul>\n<p>The <span class=\"NAVCOrange2\"><strong>Snap fPL<\/strong><\/span> (idexx.com) is a semiquantitative point-of-care test that can help rule out pancreatitis. A value of <strong><span class=\"NAVCOrange2\">&gt; 3.5 mcg\/L<\/span><\/strong> is considered positive; therefore, a positive result must be confirmed by a Spec fPL assay.<\/p>\n<p>With both tests, <em>positive results must be interpreted in light of other clinical information<\/em>, rather than considered an endpoint of diagnostic evaluation. After an episode of pancreatitis, the duration of fPL increase has not been reported.<\/p>\n<p>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.<sup><span style=\"font-size: small\">1<\/span><\/sup><\/p>\n<\/div>\n<p><strong class=\"TVPGray\">Abdominal Radiography<\/strong><br \/>\nExclusion 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.<\/p>\n<table border=\"0\" width=\"300\" cellpadding=\"5\" align=\"none\">\n<tbody>\n<tr>\n<td><span class=\"arial\">TABLE 2<br \/>\n<strong>Important Ultrasound Findings in Cats with Pancreatitis<sup>14,16-17<\/sup><\/strong><br \/>\n<\/span><\/td>\n<\/tr>\n<tr class=\"arial\">\n<td>\n<ul>\n<li style=\"text-align: left\">Increased echogenicity of mesenteric fat immediatel surrounding the pancreas*<\/li>\n<li style=\"text-align: left\">Increased pancreatic thickness (enlarged pancreas)<\/li>\n<li style=\"text-align: left\">Irregular pancreatic margins<\/li>\n<li style=\"text-align: left\">Peripancreatic free fluid<\/li>\n<li style=\"text-align: left\">Hypoechoic, hyperechoic, or mixed-echoic pancreas<\/li>\n<li style=\"text-align: left\">Mass effect in cranial abdomen<\/li>\n<li style=\"text-align: left\">Dilated common bile duct<\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<tr>\n<td class=\"references\" style=\"text-align: left\"><em>* Abnormality with highest sensitivity, based on recent study<sup>16<\/sup><\/em><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p style=\"text-align: left\">\n<h3><strong class=\"TVPGray\">Abdominal Ultrasonography<\/strong><\/h3>\n<p>Abdominal ultrasonography is a <em>key diagnostic<\/em> test in cats suspected of having pancreatitis; <strong>Table 2<\/strong> lists the most important ultrasound findings.<\/p>\n<p>The reported sensitivity of abdominal ultrasound for detecting feline pancreatitis varies widely (11%\u201368%),<sup>16<\/sup> 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.<sup>18<\/sup><\/p>\n<p>Abnormal sonographic findings are highly specific for pancreatitis\u2014a cat with compatible clinical signs and visible changes in the pancreas is very likely to be correctly diagnosed with pancreatitis (<strong>Figure 2<\/strong>).<\/p>\n<div id=\"attachment_8126\" style=\"width: 310px\" class=\"wp-caption aligncenter\"><a href=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2015\/02\/Fel-Acute-Pancr-Fig-2.png\"><img decoding=\"async\" aria-describedby=\"caption-attachment-8126\" class=\"wp-image-8126 size-full\" src=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2015\/02\/Fel-Acute-Pancr-Fig-2.png\" alt=\"Fel Acute Pancr Fig 2\" width=\"300\" height=\"203\" \/><\/a><p id=\"caption-attachment-8126\" class=\"wp-caption-text\">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. <em>Courtesy Dr. Kari Anderson, University of Minnesota Veterinary Medical Center<\/em><\/p><\/div>\n<h3><strong class=\"TVPGray\">Fine-Needle Aspiration<\/strong><\/h3>\n<p>Ultrasound-guided fine-needle aspirates of the pancreas and\/or peripancreatic tissue may assist in the diagnosis of pancreatitis (<strong>Figure 3<\/strong>), and may also be helpful when nodular changes are present.<sup>4,12<\/sup><\/p>\n<div id=\"attachment_8127\" style=\"width: 310px\" class=\"wp-caption aligncenter\"><a href=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2015\/02\/Fel-Acute-Pancr-Fig-3.png\"><img decoding=\"async\" aria-describedby=\"caption-attachment-8127\" class=\"wp-image-8127 size-full\" src=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2015\/02\/Fel-Acute-Pancr-Fig-3.png\" alt=\"Fel Acute Pancr Fig 3\" width=\"300\" height=\"230\" \/><\/a><p id=\"caption-attachment-8127\" class=\"wp-caption-text\">FIGURE 3. Pancreatic aspirate from a cat with pancreatitis (200\u00d7, Wright&#8217;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. <em>Courtesy of Dr. Leslie Sharkey, University of Minnesota Veterinary Medical Center<\/em><\/p><\/div>\n<h2>Initial Therapy<\/h2>\n<p>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.<\/p>\n<p><strong>Early IV fluid therapy with a balanced, isotonic replacement crystalloid (eg, lactated Ringer&#8217;s solution, 0.9% saline, Plasma-Lyte 156, Normosol-R)<\/strong>, 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 <em>is of critical importance<\/em>.<sup>19<\/sup><\/p>\n<p><strong>Potassium supplementation<\/strong> (up to 20\u201330 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.<\/p>\n<p><strong>Calcium gluconate<\/strong> (50\u2013150 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\u201310 mg\/kg\/H IV) are required by some cats.<\/p>\n<p><strong>Insulin therapy<\/strong> is initiated in diabetic patients.<sup>5<\/sup><\/p>\n<p><strong>Colloids<\/strong>, 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.<sup>20<\/sup><\/p>\n<p><strong>Plasma transfusion<\/strong> 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.<\/p>\n<h2>Medical Therapy<\/h2>\n<h3><span class=\"TVPGray\"><strong>Antiemetics<\/strong><\/span><\/h3>\n<p>Nausea and vomiting may be severe in patients with acute pancreatitis.<\/p>\n<ul>\n<li>The potent antiemetic <strong>maropitant<\/strong>, an NK<sub>1<\/sub> receptor antagonist, is useful for controlling emesis (and probably nausea) and providing visceral analgesia.<sup>21<\/sup><\/li>\n<li>An alternative antiemetic is a 5-HT3 antagonist (<strong>ondansetron<\/strong> or <strong>dolasetron<\/strong>), which may be combined with maropitant in severe cases.<\/li>\n<li>The dopaminergic antagonist <strong>metoclopramide<\/strong> 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.<\/li>\n<li>The histamine-2 receptor antagonist <strong>ranitidine<\/strong> may be selected for dual acid inhibition and prokinetic effects. Correction of hypokalemia also helps improve gastrointestinal motility.<\/li>\n<\/ul>\n<h3><strong class=\"TVPGray\">Gastroprotectants<\/strong><\/h3>\n<p>Gastric acid suppression is commonly incorporated into therapy for feline acute pancreatitis. The rationale includes protecting:<\/p>\n<ul>\n<li>The esophagus from exposure to gastric acid during episodes of vomiting<\/li>\n<li>Against gastric ulceration, to which patients with pancreatitis may be predisposed due to hypovolemia and local peritonitis.<\/li>\n<\/ul>\n<p>Higher gastric pH may decrease exocrine pancreatic stimulation but remains undocumented as a treatment for pancreatitis.<\/p>\n<p>When gastric acid suppression is desired, a proton-pump inhibitor (<strong>pantoprazole<\/strong>) 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.<sup>22<\/sup><\/p>\n<p>When a histamine-2 receptor antagonist is used, famotidine is believed to be most effective for suppression of gastric acid production.<\/p>\n<h3><strong class=\"TVPGray\">Analgesics<\/strong><\/h3>\n<p>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 <strong>opioids<\/strong>, such as buprenorphine or fentanyl, delivered by IV or SC injection, sublingual route, or transdermal patch.<\/p>\n<p>Convincing evidence suggests that the antiemetic <strong>maropitant<\/strong> also provides visceral analgesia.<sup>21<\/sup> Tramadol is usually avoided in cats because it can cause severe dysphoria.<\/p>\n<h3><strong class=\"TVPGray\">Antibiotics<\/strong><\/h3>\n<p>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 <em>not<\/em> routinely used.<\/p>\n<p>However, a recent study in cats using culture-independent methods<sup>9<\/sup> suggested that bacterial infection may warrant greater consideration. Coliforms are the principal pathogens, and are also seen in bile cultures from cats with cholangitis.<sup>23<\/sup><\/p>\n<h3><strong class=\"TVPGray\">Glucocorticoids<\/strong><\/h3>\n<p>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.<\/p>\n<p>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.<\/p>\n<p>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.<\/p>\n<h2>Nutritional Therapy<\/h2>\n<p>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\u2014which has come under close scrutiny in human and veterinary medicine\u2014was to &#8220;rest&#8221; the pancreas by decreasing pancreatic stimulation.<\/p>\n<p>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\u2014which attempts to maintain enterocyte integrity, reduce risk for bacterial translocation, and attenuate the systemic inflammatory response\u2014is to:<sup>24,25<\/sup><\/p>\n<ul>\n<li>Administer <strong>antiemetics<\/strong> immediately upon presentation; then as required to control vomiting<\/li>\n<li>Begin<strong> enteral feeding<\/strong> as soon as possible<\/li>\n<li>Only implement <strong>parenteral nutrition<\/strong> 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.<sup>26<\/sup><\/li>\n<\/ul>\n<p>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 <strong>Treatment Guidelines for Acute Pancreatitis in Cats<\/strong>); 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.<\/p>\n<h2><strong class=\"NAVCOrange2\">Surgical Therapy<\/strong><\/h2>\n<p>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.<sup>27<\/sup><\/p>\n<p>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.<sup>28<\/sup> Fluid accumulation within the pancreas usually resolves spontaneously.<\/p>\n<p>fPL = feline pancreatic lipase<\/p>\n<hr \/>\n<h2 class=\"arial NAVCOrange2\">In Brief: Diagnosis and Treatment of Feline Chronic Pancreatitis<\/h2>\n<p class=\"arial\"><em>P. Jane Armstrong, DVM, MS, MBA, Diplomate ACVIM, University of Minnesota, and Sarah Crain, DVM, MS, Diplomate ACVIM, Tufts University<\/em><\/p>\n<p>Chronic pancreatitis appears to be much more common in cats than acute pancreatitis (<strong>Figure 1<\/strong>).<sup>1-4<\/sup> 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) (<strong>Figure 2<\/strong>). 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.<sup>1 <\/sup><\/p>\n<div id=\"attachment_8131\" style=\"width: 310px\" class=\"wp-caption aligncenter\"><a href=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2015\/02\/Fel-Acute-In-Brief-Fig-1.png\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-8131\" class=\"wp-image-8131 size-full\" src=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2015\/02\/Fel-Acute-In-Brief-Fig-1.png\" alt=\"Fel Acute In Brief Fig 1\" width=\"300\" height=\"215\" \/><\/a><p id=\"caption-attachment-8131\" class=\"wp-caption-text\">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.<\/p><\/div>\n<div id=\"attachment_8132\" style=\"width: 310px\" class=\"wp-caption aligncenter\"><a href=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2015\/02\/Fel-Acute-In-Brief-Fig-2.png\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-8132\" class=\"size-full wp-image-8132\" src=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2015\/02\/Fel-Acute-In-Brief-Fig-2.png\" alt=\"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\u00d7 magnification. \" width=\"300\" height=\"213\" \/><\/a><p id=\"caption-attachment-8132\" class=\"wp-caption-text\">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\u00d7 magnification.<\/p><\/div>\n<h2 class=\"arial\">Diagnostic Evaluation<\/h2>\n<p class=\"arial\">Histologic features of acute and chronic pancreatitis overlap somewhat, suggesting that they may represent different points on a disease spectrum.<\/p>\n<h3 class=\"arial\"><strong class=\"TVPGray\">In the Literature<\/strong><\/h3>\n<p class=\"arial\">One necropsy-based study of 63 cats could not identify clinical features helpful in distinguishing acute from chronic pancreatitis.<sup>5<\/sup><\/p>\n<ul class=\"arial\">\n<li>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.<\/li>\n<li>Concurrent disease was common in both groups of cats, but 100% of cats with chronic pancreatitis had one or more concurrent diseases (<strong>Table<\/strong>).<\/li>\n<\/ul>\n<h3 class=\"arial\"><strong><span class=\"TVPGray\">Ultrasonography Findings<\/span><\/strong><\/h3>\n<p class=\"arial\">Ultrasonographic findings in cats with histologically confirmed chronic pancreatitis overlap considerably with findings in cats with acute pancreatitis (<strong>Table<\/strong>).<sup>5,6<\/sup> Given the clinical and histologic overlap between these forms of the disease, this is not surprising.<\/p>\n<h3 class=\"arial\"><strong class=\"TVPGray\">Fine-Needle Aspiration<\/strong><\/h3>\n<p class=\"arial\">Nodular changes may develop; fine-needle aspiration cytology may provide a useful minimally invasive method of investigation.<sup>3,7<\/sup><\/p>\n<h2 class=\"arial\">Therapeutic Measures<\/h2>\n<h3 class=\"arial\"><span class=\"TVPGray\"><strong>Nutritional Therapy<\/strong><\/span><\/h3>\n<p class=\"arial\">There is no evidence that a low-fat diet helps treat or prevent pancreatitis in cats. The authors&#8217; 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.<\/p>\n<h3 class=\"arial\"><strong class=\"TVPGray\">Medical Therapy<\/strong><\/h3>\n<p class=\"arial\">Anti-inflammatory doses of prednisolone (2.5\u20135 mg\/cat Q 48\u201372 H) are increasingly being used in cats with presumed chronic (or intermittent relapsing) pancreatitis, along with:<\/p>\n<ul class=\"arial\">\n<li>Mirtazapine on an ongoing basis as needed for appetite stimulation (mirtazapine appears to have an antiemetic effect as well)<\/li>\n<li>Maropitant at the first indication of relapse (declining appetite, apparent nausea, or vomiting).<\/li>\n<\/ul>\n<p class=\"arial\">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.<\/p>\n<div class=\"orange-box\">\n<h3>Exocrine Pancreatic Insufficiency<\/h3>\n<p>Exocrine pancreatic insufficiency is more common in cats than previously believed, and most cases are due to chronic pancreatitis.<sup>8<\/sup>Measurement of <strong>serum trypsin-like immunoreactivity (TLI)<\/strong> 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 <strong>serum cobalamin concentration<\/strong>, which can lead to various gastrointestinal and systemic complications and to treatment failure.<strong>Pancreatic enzyme supplements<\/strong> 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.<sup>2,3<\/sup> 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.<sup>2<\/sup><\/p>\n<\/div>\n<p class=\"arial\">SAMe = S-adenosyl methionine; TLI = trypsin-like immunoreactivity<\/p>\n<p class=\"TVPGray arial\"><strong>References<\/strong><\/p>\n<ol>\n<li class=\"references\">De Cock HE, Forman MA, Farver TB, et al. Prevalence and histopathologic characteristics of pancreatitis in cats. <em>Vet Pathol <\/em>2007; 44:39-49.<\/li>\n<li class=\"references\">Bazelle J, Watson P. Pancreatitis in cats: Is it acute, is it chronic, is it significant? <em>J Fel Med Surg <\/em>2014; 16:395-406.<\/li>\n<li class=\"references\">Armstrong PJ, Williams DA. Pancreatitis in cats. <em>Top Companion Anim Med <\/em>2012; 27:140-147.<\/li>\n<li class=\"references\">Xenoulis PG, Suchodolski JS, Steiner JM. Chronic pancreatitis in dogs and cats. <em>Compend Contin Educ Pract Vet <\/em>2008; 30:166-180.<\/li>\n<li class=\"references\">Ferrari JA, Hardam E, Kimmel SE, et al. Clinical differentiation of acute necrotizing from chronic nonsuppurative pancreatitis in cats: 63 cases (1996-2001). <em>JAVMA <\/em>2002; 223:469-474.<\/li>\n<li class=\"references\">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). <em>JAVMA <\/em>2014; 244:1060-1065.<\/li>\n<li class=\"references\">Crain SK, Sharkey LC, Cordner AP, et al. Safety of ultrasound-guided fine-needle aspiration of the feline pancreas: A case-control study. <em>J Feline Med Surg <\/em>2014 (epub ahead of print).<\/li>\n<li class=\"references\">Steiner JM. Exocrine pancreatic insufficiency in the cat. <em>Top Companion Anim Med <\/em>2012; 27:113-116.<\/li>\n<\/ol>\n<hr \/>\n<p>&nbsp;<\/p>\n<table border=\"0\" width=\"100%\" cellpadding=\"5\">\n<tbody>\n<tr class=\"arial\">\n<td colspan=\"3\">\n<h3><strong class=\"NAVCOrange2\">Treatment Guidelines for Acute Pancreatitis in Cats<\/strong><\/h3>\n<p><em>P. Jane Armstrong, DVM, MS, MBA, Diplomate ACVIM, University of Minnesota<\/em><br \/>\n<em> Sarah Crain, DVM, MS, Diplomate ACVIM, Tufts University<\/em><br \/>\nRead <strong>Feline Acute Pancreatitis: Current Concepts in Diagnosis &amp; Therapy<\/strong> for further details.<\/td>\n<\/tr>\n<tr class=\"arial\" bgcolor=\"#f5821f\">\n<td class=\"NAVCOrange2\"><strong>TREATMENT<\/strong><\/td>\n<td class=\"NAVCOrange2\"><strong>DOSE<\/strong><\/td>\n<td class=\"NAVCOrange2\"><strong>COMMENTS<\/strong><\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\" colspan=\"3\"><strong>1. FLUID THERAPY<\/strong><\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Balanced isotonic replacement crystalloid<\/td>\n<td style=\"text-align: left\">Maintenance at 40\u201360 mL\/kg q24h<br \/>\nAdditional replacement of ongoing losses may be required<\/td>\n<td style=\"text-align: left\">Rehydrate according to speed of losses, monitor weight and urine production, and account for cardiovascular disease<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Potassium chloride<\/td>\n<td>\n<p style=\"text-align: left\">20\u201330 mEq\/L to start; adjust depending on:<\/p>\n<ul style=\"text-align: left\">\n<li>Serum potassium values<\/li>\n<li>Fluid rate<\/li>\n<\/ul>\n<\/td>\n<td>\n<p style=\"text-align: left\">As indicated by potassium deficit:<\/p>\n<ul>\n<li style=\"text-align: left\">Replace total body losses resulting from vomiting or anorexia, or if managing diabetes<\/li>\n<li style=\"text-align: left\">Reduce in less symptomatic patients<\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Calcium gluconate<\/td>\n<td style=\"text-align: left\">50\u2013150 mg\/kg IV bolus (if symptomatic for hypocalcemia)<br \/>\n5\u201310 mg\/kg\/H IV CRI (if needed)<\/td>\n<td style=\"text-align: left\">With serial monitoring, discontinue when patient normalizes<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\" colspan=\"3\"><strong>2. ANTIEMETIC THERAPY<\/strong><\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Maropitant<\/td>\n<td style=\"text-align: left\">1 mg\/kg SC, PO, <em>or<\/em> IV q24h<\/td>\n<td style=\"text-align: left\">Refrigerate to reduce pain associated with SC injection<br \/>\nIV use is extralabel<br \/>\nProvides visceral analgesia<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Ondansetron<\/td>\n<td style=\"text-align: left\">0.5\u20131 mg\/kg IV q12-24h<\/td>\n<td style=\"text-align: left\">Administer IV injection slowly<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Dolasetron<\/td>\n<td style=\"text-align: left\">0.5\u20131 mg\/kg PO <em>or<\/em> SC q12-24h<\/td>\n<td><\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\" colspan=\"3\"><strong>3. PROKINETIC THERAPY<\/strong><\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Metoclopramide<\/td>\n<td style=\"text-align: left\">0.2\u20130.4 mg\/kg SC <em>or<\/em> PO q6-8h<br \/>\n1\u20132 mg\/kg IV\/day CRI q24h<\/td>\n<td style=\"text-align: left\">Watch for drug interactions<br \/>\nMay induce neurologic signs<br \/>\nIneffective antiemetic in cats<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\" colspan=\"3\"><strong>4. GASTROPROTECTANT THERAPY<\/strong><\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Pantoprazole<\/td>\n<td style=\"text-align: left\">1 mg\/kg IV q24h<\/td>\n<td><\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Omeprazole<\/td>\n<td style=\"text-align: left\">0.7\u20131 mg\/kg PO q24h<\/td>\n<td style=\"text-align: left\">May reduce absorption of other medications<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Famotidine<\/td>\n<td style=\"text-align: left\">0.5\u20131 mg\/kg IV <em>or<\/em> PO q12-24h<\/td>\n<td style=\"text-align: left\">Administer IV injection slowly to avoid hypotension<br \/>\nReports of intravascular hemolysis when IV used in cats<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Ranitidine<\/td>\n<td style=\"text-align: left\">1\u20132 mg\/kg IV <em>or<\/em> PO q12h<\/td>\n<td style=\"text-align: left\">Mild prokinetic effect<br \/>\nAdminister IV injection slowly to avoid hypotension<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\" colspan=\"3\"><strong>5. ANALGESIC THERAPY<\/strong><\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Buprenorphine<\/td>\n<td style=\"text-align: left\">0.005\u20130.02 mg\/kg SC, IV, <em>or <\/em>sublingual q6-8h<\/td>\n<td style=\"text-align: left\">Adverse effects uncommon<br \/>\nCan produce sedation<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Fentanyl<\/td>\n<td style=\"text-align: left\">Loading dose of 1\u20134 mcg\/kg; then 1\u20134 mcg\/kg\/H IV CRI per H<\/td>\n<td style=\"text-align: left\">Do <em>not<\/em> combine with buprenorphine or butorphanol<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Fentanyl patch<\/td>\n<td style=\"text-align: left\">12.5 mcg per H patch <em>or<\/em> 25 mcg per H patch<\/td>\n<td style=\"text-align: left\">Patch lasts 3\u20134 days once applied<br \/>\nEffect noted in 6\u201312 H<br \/>\nMay cover half of 25-mcg patch if needed<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Butorphanol<\/td>\n<td style=\"text-align: left\">0.1\u20130.2 mg\/kg per H IV CRI, after loading dose of 0.1\u20130.2 mg\/kg IV 0.2\u20130.4 mg\/kg SC, IM, <em>or<\/em> IV<\/td>\n<td style=\"text-align: left\">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)<br \/>\nIntermittent administration only may provide analgesia for 1 H or less<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\" colspan=\"3\"><strong>6. ANTIBIOTIC THERAPY<\/strong><\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Ampicillin<br \/>\nAmoxicillin<\/td>\n<td style=\"text-align: left\">10\u201320 mg\/kg IV <em>or<\/em> SC q8h<br \/>\n10\u201320 mg\/kg PO q12h<\/td>\n<td style=\"text-align: left\">Useful in combination with metronidazole<br \/>\nAmpicillin has poor bioavailability when administered orally<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Ampicillin\/amoxicillin with sulbactam<\/td>\n<td style=\"text-align: left\">20\u201330 mg\/kg IV q8h<br \/>\n62.5 mg\/cat PO q12h<\/td>\n<td style=\"text-align: left\">Sulbactam may cause diarrhea\/inappetence<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Enrofloxacin<\/td>\n<td style=\"text-align: left\">5 mg\/kg IV <em>or<\/em> PO q24h<\/td>\n<td style=\"text-align: left\">Useful in combination with metronidazole<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Marbofloxacin<\/td>\n<td style=\"text-align: left\">2.5\u20135 mg\/kg PO q24h<\/td>\n<td style=\"text-align: left\">Useful in combination with metronidazole<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Metronidazole<\/td>\n<td style=\"text-align: left\">10\u201315 mg\/kg IV <em>or<\/em> PO q12h<\/td>\n<td style=\"text-align: left\">Not suitable for use alone<br \/>\nBest in combination with aerobic\/gram-positive targeting therapy<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\" colspan=\"3\"><strong>7. NUTRITIONAL THERAPY<\/strong><\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Nutrition<br \/>\nClinicare Canine\/ Feline Liquid Diet or Vivonex (1 kcal\/mL)<\/td>\n<td>\n<p style=\"text-align: left\">Via nasoesophageal tube as:<\/p>\n<ul style=\"text-align: left\">\n<li>Continuous infusion<\/li>\n<li>Multiple small bolus feedings<\/li>\n<\/ul>\n<\/td>\n<td>\n<p style=\"text-align: left\">Achieve RER over 3\u20135 days:<\/p>\n<ul style=\"text-align: left\">\n<li style=\"list-style-type: none\">\n<ul>\n<li style=\"list-style-type: none\">\n<ul>Body<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p style=\"text-align: left\"><em>weight (kg)<sup>0.75<\/sup><\/em><\/p>\n<ul style=\"text-align: left\">\n<li style=\"list-style-type: none\">\n<ul>\u00d7 70<\/ul>\n<\/li>\n<\/ul>\n<p style=\"text-align: left\">Reduced-fat diet not indicated in cats<\/p>\n<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Mirtazapine<br \/>\n(appetite stimulant)<\/td>\n<td style=\"text-align: left\">1.88\u20133.75 mg\/cat PO Q 2\u20133 days<\/td>\n<td style=\"text-align: left\">Also has antiemetic effect<br \/>\nMain side effect is increased affection<br \/>\nSedation is dose-related<br \/>\nDo <em>not<\/em> administer with tramadol<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\" colspan=\"3\"><strong>8. OTHER THERAPIES<\/strong><\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Regular insulin<\/td>\n<td style=\"text-align: left\">Based on blood glucose monitoring:<br \/>\n0.1\u20130.2 U\/kg SC <em>or<\/em> IM q4h<br \/>\n1.1 U\/kg per day IV CRI, with or without dextrose supplementation<\/td>\n<td style=\"text-align: left\">For patients with diabetic ketoacidosis or inappetent diabetic patients<br \/>\nStrict monitoring of blood glucose required<br \/>\nPancreatitis may destabilize a previously controlled diabetic patient<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>S-adenosyl methionine (SAMe)<\/td>\n<td style=\"text-align: left\">Cats &lt; 5 kg: 90 mg PO q24h<br \/>\nCats &gt; 5 kg: 180 mg <em>or<\/em> 225 mg PO q24h<\/td>\n<td style=\"text-align: left\">Give intact tablet on an empty stomach; may be useful with concurrent liver disease<\/td>\n<\/tr>\n<tr class=\"arial\">\n<td class=\"NAVCOrange2\" colspan=\"3\"><strong>9. VITAMIN THERAPY<\/strong><\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Cyanocobalamin<br \/>\n(Vitamin B<sub>12<\/sub>)<\/td>\n<td style=\"text-align: left\">250 mcg\/cat SC weekly for 6 weeks, then 30 days later; retest after 30 days<\/td>\n<td style=\"text-align: left\">Empirical use or based on serum concentration<br \/>\nMay be useful in cats with concurrent IBD or hepatic lipidosis<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>B vitamin complex<\/td>\n<td style=\"text-align: left\">1\u20132 mL\/L of IV fluids<\/td>\n<td style=\"text-align: left\">May be useful in cats with prolonged anorexia<\/td>\n<\/tr>\n<tr class=\"arial\" valign=\"top\">\n<td>Vitamin K<sub>1<\/sub><\/td>\n<td style=\"text-align: left\">0.5\u20131.5 mg\/kg SC q12h<\/td>\n<td style=\"text-align: left\">May be useful in hyperbilirubinemic patients (ie, concurrent hepatic lipidosis)<br \/>\nUse 25-gauge needle; avoid IV use due to risk of anaphylaxis<\/td>\n<\/tr>\n<tr class=\"references\">\n<td style=\"text-align: left\" colspan=\"3\">CRI = constant-rate infusion; IBD = inflammatory bowel disease; RER = resting energy requirement<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p style=\"text-align: left\">\n","protected":false},"excerpt":{"rendered":"<p>Even though there have been advances in diagnostic capabilities, diagnosing this disease remains challenging in many cases.<\/p>\n","protected":false},"author":187,"featured_media":7,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"iawp_total_views":5581,"footnotes":""},"categories":[356],"tags":[13],"class_list":["post-6","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-january-february-2015","tag-peer-reviewed","column-features","clinical_topics-hepatology"],"acf":{"hide_sidebar":false,"hide_sidebar_ad":false,"hide_all_ads":false},"yoast_head":"<!-- This site is optimized with the Yoast SEO 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