Pancreatitis develops when there is excessive activation of trypsin and other pancreatic proteases within the pancreas, which then overwhelms local safeguards within the acinar cell. Systemic signs develop due to the activation of multiple inflammatory pathways, and local inflammation ensues due to the influx of neutrophils and the subsequent tissue damage. Despite pancreatitis being a common condition, there remains very little evidence about the best practice for treatment of the condition. For most mild to moderate cases of pancreatitis, general supportive care is likely all that is necessary. However, as the condition worsens and involves multiple organs, the mortality rate increases as does the need for intensive management.

Perfusion = Intravenous Fluid Therapy

Most dogs with acute pancreatitis (AP) require IV fluid therapy to correct fluid and electrolyte deficits. Disturbed pancreatic microcirculation is one of the earliest events in pancreatitis development and is usually multifactorial in origin. There is a theoretical benefit in using alkalinising fluids, such as lactated Ringer's solution (LRS), to increase pH and therefore prevent further trypsin activation within the acinar cell. Determination of dose rate and volume of fluids is highly variable. In animals that are only mildly affected, correction of dehydration (maintenance plus deficit) over 12 or more hours is generally sufficient. In dogs with more severe clinical signs, the current rationale is to give fluid boluses (generally ¼ blood volume over 15–20 minutes) to effect - with careful monitoring of the heart rate and blood pressure. This is a much more effective approach than giving 'shock rate' of fluids to animals, where the risk of fluid overload is high.

There are multiple rodent experimental studies that show a beneficial effect of dextrans over crystalloid therapy in AP. Dextrans administration has been associated with alteration in haemostasis and is used cautiously in dogs. That being said, additional therapy with dextrans, hetastarch, or hypertonic saline (at a low bolus dose) may be of benefit in those dogs that have severe disease and third-space loss that have not shown substantial improvement in their venous pH, serum chloride concentration, or severity of systemic inflammation at 24 hours.

Plasma

Purported benefits of plasma transfusion in treatment of AP include replacement of circulating α-macroglobulins, coagulation factors and anti-inflammatory factors. It is unlikely that any benefit seen with plasma will be due to colloid-like properties, as fresh frozen plasma (FFP) has only about 20–30% of the oncotic properties of colloids. Despite an experimental benefit of FFP in rats, there is no proven benefit in people or in dogs, and it remains an expensive treatment for veterinary patients. In the light of these findings, administration of FFP should probably be reserved for those dogs with documented coagulation abnormalities.

Analgesia

Pain is a common clinical sign of AP and is manifested in dogs typically with a crouched appearance and guarding of the abdomen on palpation. Pain is likely to be mediated due to local effects - whereby the inflamed and enlarged pancreas itself causes pain or by subsequent amplification of visceral pain. There are a number of amino acids (glutamate and aspartate) and neuropeptides (substance P, neurokinin A, calcitonin gene-related peptide) involved in a complex circuit of pain recognition and remission.

The table below is one set of recommendations for analgesia of dogs with AP, but is not tested. It is generally best to start with a high level of analgesia initially as suggested by the pain score, then reducing once pain has been well controlled rather than titrating up if pain control is ineffective. For any level of pain, gabapentin can be added as part of the multimodal approach to pain treatment. Due to the presence of hypovolaemia and dehydration in the majority of dogs with AP, NSAIDs are not recommended. There is strong experimental evidence that NK-1 receptor antagonists (such as maropitant) that reduce substance P can be useful against pain.

Nutrition

The role of nutrition in treatment of pancreatitis has gained a lot of attention recently in both human and veterinary medicine and heralded a change of direction in management. The nutritional challenges of AP include that it is a catabolic disease with significant nitrogen losses; ileus often complicates feeding; and pancreatic necrosis can increase nutritional requirements. The gastrointestinal tract itself is now also thought to be a major contributor to the systemic inflammatory state during AP, particularly if it is not supplied with luminal nutrients. Most consensus statements in human gastroenterology support the notion of early enteral feeding in severe AP, although few clinical studies effectively compare enteral nutrition to full pancreatic rest. In a prospective pilot study in dogs with severe AP, oesophageal feeding was well tolerated and safe. Large scale multicentre randomised studies are required to fully evaluate the benefits of enteral nutrition in dogs.

I currently recommend that dogs with mild-moderate pancreatitis be fasted until able to eat voluntarily, or they have reached 5–7 days of anorexia (including the pre-hospital period). In dogs with severe AP, interventional tube feeding (through a naso-oesophageal, oesophageal, or nasojejunal feeding tube) should be instituted as soon as the animal is haemodynamically stable. Feeding should be carefully introduced as the risk of regurgitation is high if the animal is obtunded. There is no current recommendation for the type of food to be administered in this acute setting; however, it seems logical to limit fat content as much as possible. Small amounts of vomiting should not stop feeding as the volume and frequency of feeds can be reduced. Careful nursing care is essential to ensure the animals are not recumbent during feeding. It is not known what percentage of resting energy requirement (RER) is necessary, but extrapolation from people would suggest that even some percentage of RER (1/4 to 1/3) spread out over 24 hours may be beneficial.

Antiemetics

Vomiting in dogs with pancreatitis is likely to be both centrally mediated due to the presence of circulating emetic agents, and peripherally mediated due to ileus, peritonitis, and pancreatic distension. There is a theoretical disadvantage in giving metoclopramide (a dopaminergic antagonist) to dogs with pancreatitis, although this is clinically unproven. Maropitant blocks the neurokinin 1 (NK1) receptor and substance P production and is an effective antiemetic agent that blocks centrally and peripherally mediated emesis. There may also be additional benefits such as reduction of visceral pain and lung injury with the use of maropitant. I currently consider maropitant as the preferred first-line antiemetic in AP and add ondansetron (0.5 mg/kg IV once then every 12–24 hours or as infusion over 6 hours) if necessary to improve nausea or emesis control. Despite the theoretical disadvantage of metoclopramide, if this combination fails to control vomiting, signs of nausea, or feeding is difficult due to ileus, then I will add metoclopramide as a continuous infusion.

Gastric Acid Suppression and Nasogastric Suctioning

Currently, there is no evidence that reducing gastric acidity improves outcome in dogs with AP. However, if there is evidence of gastric ulceration (substantial haematemesis, melena) or oesophagitis, then gastric acid suppression is indicated. Oral omeprazole, a proton pump inhibitor, has been shown to be more effective at increasing gastric pH for the longest period of time in dogs compared to famotidine, pantoprazole, and ranitidine. Dogs are often dosed with oral omeprazole at 0.7–1 mg/kg daily, but recent work would suggest that doses should be increased up to 2.5 mg/kg day, in divided doses to maintain sufficient gastric acid control. If it is not possible to give medication orally, then pantoprazole (another proton pump inhibitor) can be given intravenously.

Treatment of Local Complications

Acute fluid collection is the most suitable term for the local pancreatic complications that occur in dogs, with changes generally visible on ultrasound. Current human medical recommendations are to not surgically debride sterile fluid collections, and if infection is documented, then there should be treatment with antimicrobials for as long as possible prior to surgical debridement. Surgery to treat pancreatic acute fluid collections in dogs invariably results in a high mortality rate (> 50%), regardless of the technique used. There have been reports of spontaneous resolution of acute fluid collections in the veterinary literature and good responses to percutaneous drainage. I tend to monitor their changes only ('benign neglect') if there is no evidence of pain. However, if pain is present, then percutaneous drainage (via ultrasound guidance) is attempted.

Corticosteroids

Corticosteroids may exert multiple benefits in acute inflammation by inhibiting release of proinflammatory mediators, decreasing sequestration of neutrophils in the pulmonary vasculature, as well as reducing adhesion of primed neutrophils to the endothelial surface of pulmonary vasculature, release of elastase and free radicals from adherent neutrophils and pulmonary vascular permeability. Corticosteroids have been removed from the list of drugs that are considered to cause pancreatitis in people, and similarly they are not believed to cause pancreatitis in dogs. Currently, there are a number of prospective trials being undertaken to evaluate the potential benefit of glucocorticoids in people with severe pancreatitis. It may well be that future recommendations for treatment of pancreatitis in dogs includes corticosteroids, but at the moment there is no basis for such a recommendation.

Follow-up

Some general recommendations for treatment after discharge include:

 Remove/avoid triggers if known, especially dietary triggers.

 Provide analgesia as needed. I prefer gabapentin to tramadol due to the associated anorexia some dogs display with tramadol.

 Consider prescribing 3 weeks of pancreatic enzyme supplements as subclinical exocrine pancreatic insufficiency may be present.

 Feed a low-fat, well-balanced diet until the follow-up revisit.

 At the scheduled revisit 1–2 weeks after discharge (of course sooner if problems develop) fasting serum triglycerides and cholesterol should be measured. If the dog is not hyperlipidaemic, then transition back to their normal diet over about 4–6 weeks. If the dog is hyperlipidaemic, a low-fat diet will need to be fed for longer and underlying causes for the hyperlipidaemia such as hypothyroidism and/or hyperadrenocorticism should be screened for.

Again, these follow-up treatment recommendations are based on a poor level of evidence. It is hoped that large, multicentre studies are performed to optimise management of this common condition.