Pancreatitis: What a Pain!
British Small Animal Veterinary Congress 2008
Penny J. Watson, MA, VetMB, CertVR, DSAM, DECVIM, MRCVS
University of Cambridge, Department of Veterinary Medicine
Cambridge

Introduction

Pancreatitis in dogs and cats presents a spectrum of disease from mild, almost subclinical, to severe, acute and potentially fatal requiring intensive management. Pancreatitis may be 'acute' or 'chronic' and can also lead to diabetes mellitus (DM) and/or exocrine pancreatic insufficiency (EPI). All spectra and stages of disease present nursing challenges, not least because effective and early feeding, fluid therapy and pain management are central parts of the treatment strategy.

The Role of the Pancreas in Health

The pancreas is a rather poorly circumscribed organ next to the stomach, proximal duodenum and transverse colon. It has two principal functions: endocrine and exocrine. The endocrine function is secretion of insulin, glucagon and some other hormones into the blood from the 'islets' in response to changes in blood sugar, dietary factors and other stimuli. The exocrine function is secretion of digestive enzymes down the pancreatic duct into the duodenum. These enzymes are vital for the initial part of digestion of large molecules, e.g., lipase digests fat, amylase digests starch and trypsin digests protein. The pancreas is the only significant source of lipase so one of the key clinical signs of pancreatic enzyme insufficiency is fatty faeces (steatorrhoea).

The intestinal brush border enzymes then continue to digest these smaller molecules. The protein-digesting enzymes like trypsin would be very damaging if they were released within the pancreas, so they are packaged as inactive precursor molecules ('zymogens') within the pancreas and only activated once they reach the small intestine. Pancreatic juice is high in bicarbonate, allowing the acid stomach contents to be 'neutralised' when they enter the small intestine: the pancreatic enzymes don't work in an acid pH so this bicarbonate secretion is very important. Pancreatic juice also contains 'intrinsic factor', a substance which allows absorption of vitamin B12 (cobalamin) in the distal part of the small intestine. Without intrinsic factor, cobalamin cannot be absorbed and the animal may become deficient. This is common in EPI and can lead to atrophy and dysfunction of the gut, but can easily be treated with B12 injections. The endocrine islets comprise only about 2% of pancreatic mass whereas the exocrine tissue makes up the other 98%. In both cases, there is a large 'functional reserve'--the dog or cat has to lose about 80% of islet function before developing DM and about 90% of lipase production before developing EPI. Secretion of pancreatic juice into the duodenum is intricately coordinated with eating, digestion and the type of meal fed via nerves and local hormones and reflexes in the gut, and insulin and glucagon secretion are likewise exquisitely coordinated with food intake and enzyme secretion--the islets and acini (enzyme-secreting cells) actually 'talk to each other' in the pancreas--so it is not just coincidence that they live together.

What is Pancreatitis?

Pancreatitis is inflammation of the pancreas--which is usually sterile (NOT caused by infections). The real cause in both humans and animals is still poorly understood, which means we do not as yet have any specific treatments. The 'final common pathway' in all cases is premature activation of trypsin in the pancreas. This results literally in the pancreas digesting itself, which is very painful and can lead to local or generalised sterile peritonitis and, if severe, systemic inflammatory response, organ failure, disseminated intravascular coagulation (DIC) and death.

What causes the trypsin to activate in the pancreas in the first place? The causes in humans are finally being unraveled, whereas in dogs and cats we still often do not know the cause. Alcoholism, cystic fibrosis and gall stones are the commonest causes in people and these do not occur in dogs and cats. Other, less common, causes in humans which may have small animal equivalents are hereditary causes (e.g., due to mutations in trypsin which make it more likely to autoactivate in the pancreas) and autoimmune causes, due to autoimmune attack on the pancreatic duct. We believe the latter occurs in Cocker Spaniels in the UK. Hereditary causes may be responsible for pancreatitis in other high-risk breeds like terriers and Miniature Schnauzers, but more work is necessary to confirm this. Many of the factors previously listed as 'causes' of pancreatitis, such as high-fat diets, are probably 'trigger' factors in genetically susceptible individuals.

Pancreatitis can be 'acute' or 'chronic'. These are, strictly speaking, histological definitions: acute means necrosis, oedema and acute inflammatory infiltrate on histology. It is usually a clinically severe disease, but if the animal recovers it is completely reversible and the pancreas can become normal again (hence why it is worthwhile intensively nursing these cases). 'Chronic' disease means there is scar tissue and a chronic inflammatory infiltrate and these cases are not reversible but are often less severe. This is the major form in cats and is also common in dogs. Chronic disease can eventually lead to DM and EPI. It is difficult, if not impossible, to differentiate between acute and chronic disease clinically, particularly in cats.

How Do We Treat Pancreatitis?

Acute Pancreatitis

Acute pancreatitis is a potentially fatal disease, and we do not have specific treatments: therapy is non-specific and supportive. Mild acute pancreatitis cases could be managed at home, whereas severe cases require intensive care. How do we decide how much treatment an individual case needs? The most useful way is to use a modification of a human 'organ scoring' system developed by Ruaux. This identifies the number of organs other than the pancreas showing evidence of compromise on presentation (e.g., the kidneys may be suffering as well due to dehydration; in severe cases the liver and even lungs can be involved). The higher the number, the more likely the animal is to die and the more intensive the management necessary: dogs with organ scores of 3 or 4 probably need referral, and treatment will cost a lot of money and may not be successful. However, it is still worth trying treatment in these cases, if the owner is willing and the dog can be given adequate analgesia, because some cases will still recover completely (just not very many!). This is a clinically useful system for dogs, but has not been validated in cats and it is more difficult to predict outcome in cats since they generally 'hide' their clinical signs, even with severe disease. Cats also have a high risk of hepatic lipidosis in acute pancreatitis.

Therapy revolves around intravenous fluid therapy, analgesia and feeding. Intravenous fluid therapy is important in all but the mildest cases. It maintains hydration and perfusion of the pancreas and allows treatment of electrolyte (particularly potassium) deficits and hypoglycaemia. Urine output should be monitored and adequate. Analgesia is also vital: pancreatitis is a very painful disease. Non-steroidal anti-inflammatory drugs are generally not a good idea because of their potential for causing renal damage in a dehydrated patient and also gastric ulceration. Buprenorphine is a good choice or pethidine, or methadone can also be used. In severe pain, these may not be enough and lidocaine or ketamine infusions can be used.

Early feeding is also important. Until recently, it was believed that humans and animals with acute pancreatitis should be starved until they stopped vomiting, which was often 3-4 days or longer. However, it has now been proved in humans that early feeding improves outcome, and the more severe the pancreatitis, the earlier the feeding should be. The feeding also has to be enteral (in to the gut) and not parenteral (intravenous) to be most effective. Experimental studies in dogs suggest that early feeding is important in them, too. So how do we feed a nauseous or vomiting dog in the intensive care unit (ICU), which doesn't want to eat, into the gut? In most cases, this means anti-emetics and tube feeding. The ideal is a jejunal feeding tube, but this should be passed via a gastroscope and not placed surgically in dogs with peritonitis. Jejunal tube feeding requires constant infusion of an elemental diet. Dogs and cats can also be fed with gastrostomy or oesophagostomy tubes. A low-fat food is used (to stimulate pancreatic secretions least) and fed little and often initially; baby rice is a good start.

Chronic Pancreatitis

The major challenges in chronic pancreatitis are diet and analgesia. It is easy to underestimate the pain in chronic pancreatitis. Again, finding a suitable analgesic for outpatient use can be challenging. In many cases, just changing to a low-fat diet is very effective at reducing postprandial pain. Most dogs and cats with DM and chronic pancreatitis do remarkably well long term, in spite of an inherent 'instability' in their management associated with recurrent flare-ups in disease. In most cases, they should NOT be fed a calorie-restricted diet but rather a low-fat intestinal-type diet.

References

1.  Meier RF, Beglinger C. Nutrition in pancreatic diseases. Best Practice and Research Clinical Gastroenterology 2006; 20(3): 507-529.

2.  Ruaux CG, Atwell RB. A severity score for spontaneous canine acute pancreatitis. Australian Veterinary Journal 1998; 76: 804-808.

Speaker Information
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Penny J. Watson, MA, VetMB, CertVR, DSAM, DECVIM, MRCVS
University of Cambridge
Department of Veterinary Medicine
Cambridge, UK


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