Nutritional Management of Pancreatitis in Dogs
Historically, it has been advocated to “rest” the pancreas during bouts of acute pancreatitis by withholding enteral nutrition to avoid stimulation of the exocrine pancreas and the risk for continued premature zymogen activation.3-6 Supporting evidence for this practice is minimal, and several studies challenge it.6 Evidence is mounting that early enteral nutrition improves clinical outcomes in systemically ill patients.3,4,7,8 Specifically, early enteral nutrition has been shown to decrease ileus and inflammation, stimulate intestinal mucosal regeneration and mucosal blood flow, decrease protein catabolism, and prevent protein-energy malnutrition.4,6,9 A recent retrospective study of 34 dogs with acute pancreatitis concluded that early enteral nutrition (i.e., within 48 hours of hospitalization) had a positive effect on return to voluntary food intake, was associated with less gastrointestinal intolerance, and should be considered as part of medical management.4
Imposed anorexia may be counterproductive to overall gastrointestinal health, as avoidance of enteral nutrition has been correlated with increased gastrointestinal permeability, bacterial or endotoxin translocation, and immunosuppression.3,6,10 Increased metabolic demands, protein catabolism, and bacterial translocation associated with pancreatitis itself may lead to systemic inflammatory response syndrome (SIRS).10
At the author’s hospital, nasoesophageal and nasogastric tubes are often used in management of patients with acute pancreatitis. Placement of a feeding tube is relatively inexpensive and generally well tolerated. Syringe feeding is not recommended based on its practical inability to deliver full nutrient requirements and the risk of food aversion and aspiration.5
Ideally, hospitalized dogs should be fed their estimated resting energy requirement (RER) based on either 70 × (body weight in kg)0.75 = RER (kcal/day) or [30 × (body weight in kg)] + 70 = RER (kcal/day). The first formula is the more accurate of the two and is used at the author’s institution for dogs weighing <5 kg or >25 kg, while the second is an approximation of RER for dogs weighing 5 to 25 kg.1,5 In patients that cannot tolerate their full RER as enteral nutrition, providing at least part of the RER via this route will likely provide some benefit in maintaining the absorptive surface area of the intestines.5
Liquid enteral diets designed for veterinary use are available (TABLE 2). Human enteral diets may be used for short-term feeding, but their lower fat, protein, and essential nutrient profiles make them inappropriate for long-term use.5
Vomiting and nausea-associated inappetence are common in patients with acute pancreatitis, and antiemetics are commonly used for their management. These signs are likely to be mediated centrally by circulating emetic agents and peripherally by ileus, peritonitis, and pancreatic destruction.3 Several antiemetics are routinely used for management and are considered effective and useful, although few have been subjected to rigorous testing;11 common choices are listed in TABLE 1.
Maropitant, an NK₁ (neurokinin-1) receptor antagonist, is a first-line antiemetic that acts both centrally (i.e., chemoreceptor trigger zone and vomiting center) and peripherally (gastrointestinal tract).1,3,12,13 Maropitant has been found to be superior to metoclopramide for management of peripherally stimulated vomiting.13 Rodent studies have suggested that, in addition to its antiemetic action, maropitant may inhibit inflammation by blocking NK₁ receptors in the pancreas.12,14 Other antiemetic agents with proposed anti-inflammatory activity, such as serotonergic antagonists (e.g., ondansetron), can be added as necessary to improve nausea and control emesis.1
At the author’s institution, maropitant is the preferred antiemetic. For dogs that are refractory to this medication, metoclopramide (1 to 2 mg/kg q24h as a constant-rate infusion) or ondansetron (0.1 to 1.0 mg/kg q6h to q12h) is used as additional supportive therapy.
Proton pump inhibitors (e.g., omeprazole, pantoprazole) and histamine type-2 (H2) receptor antagonists (e.g., famotidine, ranitidine) are useful adjunctive medications and may decrease the risk of gastric or intestinal ulceration or esophagitis (TABLE 1).
Reduction of gastric acidity is frequently recommended during treatment for acute pancreatitis, although no evidence is available that shows reduction of gastric acidity leads to decreased pancreatic exocrine stimulation or improved outcome in dogs with acute pancreatitis.1,3,15 However, if there is clinical evidence of gastric ulceration (hematemesis or melena) or esophagitis (repeated eructation, regurgitation), then gastric acid suppression is indicated.1
When used twice a day, proton pump inhibitors are superior to H2-antagonists for raising the intragastric pH.1,16,17 No greater effect is exhibited with the short-term combination of H2-antagonists and proton pump inhibitors compared with use of either drug class alone.18
A disturbance in pancreatic microcirculation plays a central role in the pathogenesis of acute pancreatitis and the transformation from acute, self-limiting to severe, necrotizing pancreatitis.1,3,19 The pancreatic microcirculation can be disturbed by many factors, including hypovolemia, dehydration, increased capillary permeability, and microthrombi.1,3,19
The rationale for intravenous fluid therapy is to replenish blood volume and thus blood flow to the pancreas, with several animal studies demonstrating both improved pancreatic circulation and survival with fluid resuscitation.20,21 However, pancreatic blood flow and oxygen consumption are not completely restored with fluid resuscitation alone.21 Little information is available pertaining to the best initial fluid choice; however, an isotonic fluid (e.g., lactated Ringer’s solution, 0.9% sodium chloride) is appropriate. The fluid plan should incorporate the estimated fluid deficit, any ongoing losses (i.e., vomiting, diarrhea), and the ongoing maintenance requirement. Electrolytes should be monitored and supplemented accordingly.
Crystalloid therapy alone may not be adequate in dogs with severe acute pancreatitis.3 Colloid fluid administration has been studied in people with pancreatitis, with improved outcomes found compared with crystalloid resuscitation.19 The current role of colloid solutions in pancreatitis management in veterinary patients is controversial. Several human studies and a recent veterinary study have suggested that there is an increased risk of renal dysfunction, coagulation/platelet dysfunction, and mortality with the use of colloids.22-24 Additional prospective longitudinal studies in veterinary medicine are warranted to investigate the increased risks (e.g., acute kidney injury) associated with colloid administration in critically ill patients.
Diagnostic Approach
Initial workup included a complete blood count (CBC), serum biochemical profile, urinalysis, urine culture, coagulation panel, and patient-side SNAP cPL test (idexx.com); the results of the CBC, serum biochemical profile, and coagulation panel are shown in Tables 3 and 4, with abnormal results bolded. Blood and urine samples were collected before treatment was initiated.
In addition, 3-view abdominal radiographs were taken to rule out a gastrointestinal (GI) foreign body and other obvious abdominal organ-related diseases. On the basis of abdominal radiography results, abdominal ultrasonography with abdominocentesis was performed. The collected abdominal fluid was prepared for analysis and cytology.
Plasma Transfusion
The proposed advantage of using plasma in dogs with acute pancreatitis includes supplementation of alpha-2-macroglobulin (scavenger proteins for activated proteases in serum), coagulation factors, and anti-inflammatory factors.20 Due to the high cost and lack of confirmed benefits in dogs, however, plasma transfusion is generally reserved for dogs suspected to have DIC.
Pancreatitis in the dog. Dr. Dan explains.
Located by the stomach, the pancreas makes and releases enzymes that aid in digestion. Normally, these enzymes are not active until they reach the small intestine. However, with pancreatitis the enzymes activate too early and irritate the pancreas and surrounding tissue. This leads to pancreatitis, or inflammation of the pancreas.
Pancreatitis is often an acute problem causing gastrointestinal signs of vomiting and/or diarrhea along with abdominal pain that can progress rapidly. Recurrent bouts can have long–term consequences including repeated hospitalizations and development of chronic pancreatitis. Early diagnosis and treatment are therefore recommended to prevent complications and improve your pet’s quality of life.
In most cases, the cause of pancreatitis is unknown in both cats and dogs. Some pets experience acute pancreatitis, meaning it comes on suddenly. Other pets have chronic pancreatitis where it develops over time. Both types can range from mild to severe and can be quite painful.
Clinical presentation in cats and dogs can be nonspecific. Patients with acute pancreatitis often present for gastrointestinal signs of vomiting, diarrhea, abdominal pain, distended abdomen, dehydration, fever, and yellow tinge to their eyes, inner ears, or skin. Patients with chronic pancreatitis may have mild signs including anorexia, decreased appetite, and lethargy.
Due to the nonspecific nature of the signs, diagnosing pancreatitis includes ruling out other causes of anorexia, vomiting, diarrhea, and abdominal pain. It is important to let your veterinarian know about all the medications that your pet may be on to ensure those aren’t causing the symptoms. Your pet may also be tested for other diseases if there is clinical suspicion. Take note of and discuss symptoms like increased drinking, increased urination, changes in energy level, hair loss, and weight changes (loss or gain) with your veterinarian. These may be helpful to diagnose other conditions.
Your veterinarian will typically perform abdominal radiographs (X-rays) first to rule out gastrointestinal foreign bodies. Patients with pancreatitis can show some mild changes on abdominal X-rays, however abdominal ultrasound is often necessary for diagnosing pancreatitis.