Mrs. Williams is on the phone concerned about her 7-year-old Yorkshire terrier, Max, who hasn’t eaten in two days and has been vomiting and having diarrhea for the last 24 hours. This morning Mrs. Williams reports that Max is quite weak and seems to be uncomfortable—he isn’t able to rest. You advise Mrs. Williams to bring Max in right away for an evaluation.
On presentation, Max is dehydrated, drooling and licking his lips. Even though he’s weak, he cries and tries to bite the doctor during abdominal palpation. During history collection, Mrs. Williams tells you Max got into the garbage three days ago—garbage that contained bacon grease from the Williams’ breakfast that morning.
There are likely to be a number of conditions on your veterinarian’s differential diagnosis list, and pancreatitis should be near the top.
The pancreas is a glandular organ with both endocrine and exocrine functions. As an endocrine gland, the pancreas is responsible for maintaining blood glucose levels by producing and secreting two hormones: insulin to lower blood glucose and glucagon to increase blood glucose. These hormones are produced in pancreatic beta and alpha cells, respectively.
As an exocrine gland, the pancreas creates and secretes the digestive enzymes amylase and lipase, as well as trypsinogen, the precursor to trypsin, which is the primary digestive enzyme for proteins (also known as a “protease”). Trypsinogen is a zymogen, an inactive enzyme form that requires activation to function. Digestive zymogens and enzymes are secreted in response to the presence of chyme in the duodenum, as occurs after a meal; they are required for proper digestion of food as it enters the small intestine.
Under normal circumstances, trypsinogen is not activated to trypsin until it comes into contact with enterokinase, an enzyme produced by the brush border cells of the duodenal lumen. This separation protects pancreatic tissue from exposure to proteases, preventing the breakdown of proteins within the pancreas and other organs.
However, if trypsin is instead activated within the acinar cells of the pancreas—possibly due to oxidative stress, excess stimulation of the cells from high-fat diets,1 or hypotension2—it leads to autodigestion and inflammation. The local inflammation draws an influx of neutrophils and macrophages, which release additional inflammatory cytokines such as tumor necrosis factor, interleukins, platelet-activating factor and nitric oxide.
As these cytokines are activated and circulate throughout the body, severe pancreatic damage can lead to a systemic inflammatory reaction known as systemic inflammatory response syndrome (SIRS), characterized by increased capillary permeability, fever, tachycardia and hypotension and culminating in multiple organ dysfunction syndrome (MODS).3
Activation of trypsinogen within the pancreas triggers activation of the zymogens of other proteases as well, increasing the risk and rate of autodigestion. If this autodigestion continues unabated, patients may develop severe necrotizing pancreatitis, wherein portions of the pancreas are completely destroyed. In humans, the reported mortality rate due to pancreatitis is 5% to 15%, and in dogs it is reported to be much higher, ranging from 27% to 58%.2
The exact cause of pancreatitis is multifactorial and often unknown, and there is much discussion in the literature about potential causative conditions and agents that may lead to pancreatitis in canine patients. The list of patient-based risk factors for the development of pancreatitis includes:
- Diabetes mellitus
- Pre-existing gastrointestinal disease
- Middle or older age
- Small breed.
About 25% of dogs presenting to their veterinarian with acute diabetes mellitus also have acute pancreatitis.1 Pancreatitis is also more common in dogs that have had surgery—particularly in the abdominal cavity—within the past two weeks. In addition, dietary indiscretion (with or without the presence of hyperlipidemia) has been implicated often in acute pancreatitis. High-fat foods that are traditionally thought of as triggers for pancreatitis (such as bacon grease, fatty meats, turkey skin and so on) are not the only contributors; any food outside a dog’s normal diet may also lead to pancreatic inflammation. Numerous drugs have also been implicated in pancreatitis induction, including azathioprine, thiazides, furosemide, tetracycline, potassium bromide and L-asparaginase.1
Many breeds have a predisposition to developing pancreatitis (see the list at right). Miniature schnauzers in particular are prone to increased serum levels of cholesterol and triglycerides, manifesting as hyperlipidemia, which may contribute to their susceptibility to pancreatitis. It isn’t known whether circulating levels of lipids in the bloodstream cause pancreatic damage, leading to pancreatitis, or if the hyperlipidemia is secondary to pancreatitis and a subsequent inability to properly metabolize lipids.1
In a 2011 study, miniature schnauzers that had recovered from acute pancreatitis were five times more likely to exhibit hyperlipidemia after clinical recovery than a control group of miniature schnauzers that did not have pancreatitis.4 Prepancreatitis blood samples were not available in this study, so it is unknown if high levels of circulating triglycerides were the causative agent or a secondary sequela. But it is clear that pancreatitis is a multifactorial pathologic process potentially with both genetic and environmental triggers playing a role.
Next: Presentation and clinical signs
Presentation and clinical signs
Patients can present with varied and nonspecific clinical signs ranging from mild to very severe. In a 1999 case series published in the Journal of the American Veterinary Medical Association,5 signs seen in patients with acute pancreatitis confirmed via histopathology performed at necropsy included:
- anorexia (91%)
- vomiting (90%)
- weakness (79%)
- abdominal pain (58%)
- dehydration (46%)
- diarrhea (33%).
In severe cases, the inflammation may become systemic and patients may present in shock or cardiovascular collapse. On physical exam, the most common findings are dehydration, ptyalism and other signs of nausea (lip-licking, grimacing and so on), and cranial abdominal pain. Because the signs are nonspecific, a thorough diagnostic workup is indicated, including bloodwork and imaging.
The first step in any good diagnosis, of course, is gathering a complete and accurate history and performing a thorough physical exam. As in the case of Max, the Yorkshire terrier described above, an owner may disclose a dietary indiscretion that helps narrow the diagnostic path for the clinician, but often the clinical signs point to many potential disorders—including simple gastroenteritis, foreign body obstruction or peritonitis—and the history provided may or may not be helpful.
The next step in diagnosing pancreatitis is to perform bloodwork. A serum chemistry profile, including electrolytes, and a complete blood count (CBC) are indicated. Many patients will be azotemic (showing increased blood urea nitrogen [BUN] and creatinine levels) secondary to dehydration. Also characterized as a prerenal azotemia, the increase in BUN and creatinine is secondary to decreased blood flow through the kidneys due to hypovolemia, leading to a decrease in the kidneys’ ability to excrete these waste products.
Often these patients will have increased liver enzymes, which can be attributed to pancreatic inflammation narrowing the common bile duct and causing hepatic enzymes to congest the liver rather than be excreted into the intestinal tract. If the common bile duct is obstructed or narrowed, bile cannot flow out of the canaliculi, leading to an increase in circulating serum levels of liver enzymes as they move into the bloodstream instead of through the bile duct. If this blockage or narrowing is not corrected, bile may not be able to flow normally out of the gallbladder, overloading its normal storage capacity and potentially resulting in cholecystitis.
Because pancreatitis and diabetes mellitus occur together with some regularity, hyperglycemia and hypokalemia are common abnormalities as well. Patients with septic processes (septic peritonitis, for example) may also have hypoglycemia, so the full clinical picture is important to keep in mind.
The acid-base status in these patients can vary along with clinical signs. In severe cases, the patient may have a metabolic acidosis evident on blood gas analysis. However, if vomiting has been severe or protracted, the patient may have a metabolic alkalosis instead due to the loss of hydrochloric acid required for normal digestion.
The CBC will usually show an elevated packed cell volume (PCV) due to dehydration-induced hypovolemia, an inflammatory leukogram (characterized by neutrophilia, monocytosis and lymphopenia), and thrombocytopenia, particularly in severe cases. If the patient has a lower-than-normal platelet count, the veterinary team must be on guard for the development of disseminated intravascular coagulation (DIC), a potentially lethal complication of pancreatitis.
Most patients with pancreatitis show elevations in their serum amylase and lipase levels, which may be attributed to decreased excretion of these substances by the kidneys, due to decreased flow through the kidneys secondary to hypovolemia. For many years serum amylase and lipase values were used as markers of pancreatitis on bloodwork. However, increased levels of these enzymes are not specific to pancreatitis, because many other organs in the body also synthesize and secrete amylase and lipase.
In recent years, Texas A&M University has developed a test for canine pancreatic-specific immunoreactivity, also known as the Spec cPL, which measures only lipase that comes from the pancreas; this test is highly sensitive (93%) and moderately specific (78%).6 (See “Specificity vs. sensitivity” at right for an explanation of sensitivity and specificity in laboratory tests.) Abaxis has recently introduced a point-of-care cPL test that offers semiquantitative results almost immediately, without the necessity of submitting to an outside lab.
Also available is the SNAP cPL test from IDEXX; however, this test provides the veterinary team only with a qualitative abnormal/normal value. For example, if the patient has an initial cPL value of 800 mcg/L (normal = < 200 mcg/L) and, after two days of therapy (see the treatment section on the next page), the value has decreased to 300 mcg/L, there’s been good progress in reducing the amount of pancreatic lipase circulating in the patient’s bloodstream. However, comparing SNAP cPL values in the same patient over the same timeframe would simply show two abnormal results, meaning the pancreatic lipase levels are somewhere above 200 mcg/L, making it not as useful for tracking your patient’s progress. While both the quantitative and semiquantitative cPL tests provide a number value, higher values do not necessarily correlate to disease severity. Remember: We treat patients, not numbers!
Pancreatitis cannot be diagnosed solely on the basis of any one test but must take into account the entire clinical presentation. Imaging plays a key role. Ultrasound is the primary imaging modality used to help confirm the diagnosis, though recent studies have shown moderate-to-low agreement between ultrasonographic diagnosis of canine pancreatitis and Spec cPL values.7 This may be due to interoperator differences in ultrasound skill and technique. Because the clinical signs seen at presentation can be nonspecific, a full ultrasound examination of the abdomen is warranted to rule out other differential diagnoses like foreign body obstruction or peritonitis. Abdominal radiographs can also be performed, but they’re often not as helpful as ultrasound examination.
Histopathology performed on biopsies of the pancreas has been shown to definitively diagnose pancreatitis, but surgery is an invasive diagnostic tool and often cost-prohibitive. However, fine needle aspirates (FNA) of the pancreas for cytologic examination do have diagnostic value based on a 2015 retrospective study.8 Patients in that study also had a very low rate of complications (6.3%), and the diagnostic yield of cells was high. In several of the study subjects, histology from surgical biopsy was also available, and cytologic examination was found to correlate well with histologic examination (11/12 had complete agreement between the two examinations).
Historically, clinicians have been concerned that performing FNAs of the pancreas may lead to further cellular damage and subsequent pancreatic enzyme elevations. However, it has been shown that sampling the pancreas via FNA does not lead to an increase in measured pancreatic enzymes, which might confound a diagnosis or lead to difficulties in monitoring treatment progress.9 In addition to the relative ease of sample collection via FNA (as opposed to surgical biopsy), the low complication rate is superior to the complication rate found in postsurgical patients (29% in a 2014 retrospective study).10 In cases where pancreatitis is accompanied by comorbidities—such as pancreatic abscesses identified on ultrasound, septic peritonitis or biliary obstruction—surgical intervention is warranted and pancreatic biopsies should be taken as part of the surgical procedure.
Many of the following supportive care actions may be taken regardless of diagnosis when a systemically ill and dehydrated patient presents to the veterinary hospital. Once pancreatitis has been confirmed, the veterinary team should pursue appropriate treatment quickly to provide improved intravascular volume, better perfusion and oxygen delivery, analgesia, nausea reduction and nutrition. There is no definitive curative procedure or medication for acute pancreatitis—treatment is supportive and aimed at reduction of clinical signs.
Treatment of comorbidities identified during diagnosis should proceed alongside supportive efforts up to and including surgery if indicated. While empiric treatment of clinical signs is often successful in veterinary medicine, the veterinary team should strive to obtain a definitive diagnosis through the means outlined above.
Intravenous fluid therapy. Dehydration, hypovolemia and electrolyte imbalances must be addressed early in the patient’s presentation. Dehydration deficits can be replaced in the first 24 to 48 hours after presentation using intravenous (IV) isotonic buffered crystalloid solutions such as Plasma-Lyte A (Baxter), Normosol-R (Hospira) or lactated Ringer’s solution (LRS). Correcting dehydration and hypovolemia will improve blood flow to the kidneys, allowing normalization of kidney perfusion and function and excretion of BUN, creatinine, amylase and lipase. IV fluid therapy will also improve pancreatic perfusion, helping to restore normal function.
In cases where hypokalemia is present, potassium supplementation should be added to the IV fluid therapy plan. IV fluids can also help correct acid-base abnormalities by restoring perfusion and oxygen delivery to the tissues. In patients with septic processes (such as septic peritonitis), additional blood pressure and perfusion support may require colloid administration. Recent evidence encourages clinicians to exercise caution when using synthetic colloids in septic patients due to the potential risk for kidney injury.11,12 Many practitioners reach for fresh frozen plasma (FFP) to replenish protein levels, improve oncotic pressure and replace protease inhibitors lost due to consumption. A 2009 study showed no survival benefit to using FFP to treat pancreatitis,13 but its use is certainly indicated in patients with evidence of coagulopathies or DIC.1
Analgesia. Even if patients show no obvious signs of abdominal pain, analgesics should be administered to any dog diagnosed with pancreatitis. Ninety percent of people suffering from acute pancreatitis report high levels of pain,14 and we can extrapolate from that information that our veterinary patients are also painful, even if we cannot detect it on physical exam or observation. Buprenorphine at 0.01-0.05 mg/kg IV, IM or via the oral-transmucosal route (OTM) can be used for mild to moderate pain. Fentanyl is an excellent choice for patients with moderate to severe pain. Fentanyl must be delivered via constant rate infusion (CRI) due to its short half-life in dogs (approximately 45 minutes);15 doses range from 2-10 mcg/kg/hr, depending on the level of analgesia needed.1
If fentanyl is not sufficient to manage the patient’s pain, lidocaine (5-30 mcg/kg/min), ketamine (0.1-0.6 mg/kg/hr) or both may be added. In patients whose pain cannot be controlled with systemic analgesics, veterinary teams should consider an epidural or intra-abdominal or intrathoracic analgesia. A 2013 study in pigs demonstrated that administration of thoracic epidural analgesia resulted in better tissue perfusion and improved survival in experimentally induced acute pancreatitis.16 In human patients, studies have demonstrated that epidural analgesia increases perfusion to the pancreas and improves clinical outcomes in patients with acute pancreatitis while reducing the severe pain associated with the condition.17
Anti-emetic therapy. Anti-emetic therapy helps increase patient comfort and reduces ongoing fluid losses. Maropitant (Cerenia—Zoetis) is an effective anti-emetic with both central and peripheral effects. It can be given IV or subcutaneously (SC) at 1 mg/kg every 24 hours or orally at 2 mg/kg every 24 hours. Maropitant can be painful on SC injection, but in my experience, refrigerating the drug appears to minimize the pain felt on injection.
Maropitant is also an excellent choice because, in addition to being an effective anti-emetic, it is a neurokinin-1 antagonist that blocks the action of substance P. Substance P is produced by nerves systemically and is involved in increasing inflammation, nociception and vascular permeability throughout the body. Blocking substance P may decrease visceral pain, reduce the severity of pancreatitis and minimize its systemic effects.18 If maropitant is not sufficient to control nausea or vomiting, ondansetron (Zofran—GlaxoSmithKline) may be added to the treatment plan at 0.1-0.2 mg/kg IV every 12 hours.19
Nutrition. Early enteral nutrition is an important part of successful treatment of acute pancreatitis. Traditionally patients with pancreatitis have been ordered to have nothing by mouth for several days while hospitalized, but studies have shown that adequate nutrition, beginning as early as possible in the course of the disease, improves survival. Pancreatitis is a catabolic process wherein the body is actively destroying its own tissues to provide nutrients for cellular processes. By definition, catabolism consumes energy; by supplying exogenous energy in the form of nutrition, we can reverse the catabolic process and allow the body to return to homeostasis.20 Additionally, by supplying nutrients to the lumen of the gastrointestinal tract, we are feeding and supporting the enterocytes, preserving gastrointestinal barrier function, intestinal motility and the normal flora of the gut.21
A recent retrospective study in the Journal of the Veterinary Emergency and Critical Care Society investigated the impact of providing enteral nutrition within 48 hours of hospitalization for acute pancreatitis. The researchers found that providing patients with enteral nutrition early in the course of their hospitalization led to a faster return to voluntary eating and a fewer incidences of both regurgitation and vomiting.22 On average, patients in this study were already hypo- or anorexic for 72 hours before their admission to the hospital.
In patients that have not been eating—or that are expected not to eat—for a period of 72 hours, consider placing a feeding tube. Nasogastric or nasoesophageal tubes can be placed in practice with little to no sedation or anesthesia needed. These tubes can be used to provide liquid nutrition (such as CliniCare—Zoetis or Emeraid—Lafeber) either via bolus feedings or continuous trickle feeding while patients are in the hospital. If a feeding tube will be needed after discharge from the hospital to ensure adequate caloric intake, consider placing an esophageal feeding tube as long as the patient can tolerate a short anesthetic procedure. Esophageal feeding tubes can accommodate a larger variety of diets, enabling clients to feed a more calorically dense food to meet a patient’s nutritional needs.
The best choice of diet for pancreatitis patients is one that is highly digestible, meaning it breaks down into key nutritional factors that are readily absorbed. It was once thought that ultra-low-fat diets were most appropriate in pancreatitis cases, but studies have not demonstrated harm related to fat consumption in enteral nutrition. However, in patients with hyperlipidemia, it’s still best to choose a diet lower in fat.21 Another consideration is the caloric density of the food—choose a diet that will meet a patient’s resting energy requirement (RER) in a reasonable volume of food. To calculate a patient’s RER, use the following formula:
(Body weight in kg)0.75 x 70 = total kilocalories (kcal) required per day21
If a patient has not eaten for three or more days before presentation to the hospital, start feeding slowly; target one-third of RER on day one of enteral feeding and increase gradually until full RER has been reached. Provide bolus tube feedings every four to six hours, depending on the patient’s tolerance. Increase volume or frequency only if the patient is tolerating feeding well, with no signs of nausea and no vomiting. In patients that cannot tolerate enteral nutrition, as evidenced by intractable vomiting, consider parenteral nutrition. Parenteral nutrition requires specialized catheters as well as production facilities and is not generally feasible in general practice—referral to a specialty center may be necessary in these cases.
Other therapies. Prophylactic antibiotic therapy has not been shown to increase survivability in human studies,23 and infection is rarely a cause of acute pancreatitis in dogs. However, in experimentally induced canine pancreatitis, treatment with broad-spectrum antibiotics improved survival.1 It is prudent for clinicians to practice good antibiotic stewardship and consider whether antibiotics are needed on a case-by-case basis. If presence of infection is demonstrated, antibiotic therapy is definitely indicated.
Avoid both steroids and nonsteroidal anti-inflammatory drugs (NSAIDs) in cases of acute pancreatitis. NSAIDs have been implicated as a class of pharmaceuticals with the potential to induce pancreatitis, and steroids have not shown any benefit in human studies.14
Next: Client education and home care
Client education and home care
Dogs that experience acute pancreatitis may recover fully, may suffer a relapse of acute pancreatitis, or may clinically recover but suffer from chronic pancreatitis. In cases where comorbidities are present—such as diabetes, hyperlipidemia or other disease states—the success of pancreatitis treatment will depend on successful treatment or management of the other disease process.
When patients are discharged after an incidence of acute pancreatitis, clients will need guidance on what to feed and signs to look for that may indicate a recurrence of clinical disease. Counsel clients to avoid feeding unusual foods, table scraps or high-fat treats or foods to their dogs. Recommend diets that are highly digestible, with high-quality ingredients and low amounts of fat. For patients that are not hyperlipidemic at discharge, veterinary nutritionists recommend targeting a diet that contains 15% fat or less and 15% to 30% protein in the convalescent diet, as measured on a percentage dry matter basis.20 For patients with evidence of hyperlipidemia, diets should contain 10% fat or less; the protein level recommendations remain the same.20 See Table 1 for a list of recommended diets.
Table 1: Suggested veterinary diets for dogs with acute pancreatitis*
|Fat percentage (target 15% or less)||Protein percentage (target 15-30%)|
|Hill’s i/d Low Fat||8.3%||24.5%|
|Purina EN Gastroenteric||10.0%||32.0%|
|Royal Canin Gastrointestinal Low Fat||4.2%||25.0%|
|Purina EN Gastroenteric||11.9%||26.0%|
|Royal Canin Gastrointestinal Low Fat||4.5%||20.0%|
|Royal Canin Gastrointestinal Moderate Calorie||10.0%||23.0%|
*Nutrients expressed as a percentage of dry matter.
Adapted from Hand MS, Thatcher CD, Remillard RL, et al., eds. Small animal clinical nutrition. 5th ed. Topeka, KS: Mark Morris Institute, 2010.
What about Max?
After a full physical examination, the veterinarian orders blood work to check serum chemistries and submit to the reference lab to check a cPLi. The veterinarian also performs an ultrasound and finds evidence of an inflamed pancreas. Max is admitted to the hospital for IV fluid therapy, pain control, anti-emetic medications and nutritional support.
After three days of supportive care, Max is eating well on his own, with no further vomiting, and is no longer painful. He is discharged for continued at-home care by the grateful Mrs. Williams. You remind Mrs. Williams to avoid high-fat foods for Max and to notify your office if he gets into any more bacon grease in the future. You also educate her on the signs that would indicate Max is having a recurrence of pancreatitis (vomiting, inappetance, evidence of pain).
With diligent monitoring and supportive care, both in the hospital and at home, dogs can make a full recovery from acute pancreatitis.
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Hayes G, Benedicenti L, Mathews K. Retrospective cohort study on the incidence of acute kidney injury and death following hydroxyethyl starch (HES 10% 250/0.5/5:1) administration in dogs (2007-2010). J Vet Emerg Crit Care 2016;26(1):35-40.
Weatherton LK, Streeter EM. Evaluation of fresh frozen plasma administration in dogs with pancreatitis: 77 cases (1995-2005). J Vet Emerg Crit Care 2009;19(6): 617-622.
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Sano T, Nishimura R, Kanazawa H, et al. Pharmacokinetics of fentanyl after single intravenous injection and constant rate infusion in dogs. Vet Anaesth Analg 2006;33(4):266-273.
Bachmann KA, Trepte CJC, Tomkotter L, et al. Effects of thoracic epidural anesthesia on survival and microcirculation in severe acute pancreatitis: A randomized experimental trial. Crit Care 2013;17(6):doi:10.1186/cc13142.
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Pastor CM, Frossard JL. Are genetically modified mice useful for the understanding of acute pancreatitis? FASEB J 2001;15(6):893-897.
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