Canine Acute Pancreatitis Ladan Mohammad-Zadeh ... - DoveLewis

Canine Acute Pancreatitis 

Ladan Mohammad-Zadeh, DVM DACVECC 

Speaker Notes 

Pancreatitis was first described by Dr. Reginald Fitz in 1889. Dr. Berkeley Moynihan in 

1925 wrote of pancreatitis: “Acute pancreatitis is the most terrible of all the calamities 

that occur in connection with the abdominal viscera. The suddenness of its onset, [and] 

the agony which accompanies it…render it the most formidable of catastrophies” Annal 

of Surgery. It was recognized early on as a devastating disease process. Surgical 

intervention was the standard of care in the early 20th century. Fallis in 1939 

demonstrated that patients treated surgically had higher mortality rate (46%) than those 

treated medically (5%). Although diagnosis and treatment of pancreatitis have improved, 

the link between etiology and pathogenesis is still poorly understood. 

The body of the pancreas likes at the pylorus, the right lobe lies along the descending 

duodenum, and the left lobe lies along the greater curvature of the stomach in the greater 

omentum. The ductal system in the dog consists of 2 ducts; the pancreatic duct, which 

lies adjacent to the common bile duct just before it enters the duodenum through the 

major duodenal papilla and the accessory pancreatic duct which enters the duodenum at 

the level of the minor duodenal papilla. 80% of cats lack an accessory pancreatic duct 

and the pancreatic duct will often join the common bile duct prior to opening into the 

major papilla. 

The pancreas has endocrine and exocrine functions. The endocrine function lies in the 

Islet of Langerhans. Here the alpha cells secrete glucagon, beta cells secrete insulin, and 

delta cells secrete somatostatin. These hormones are secreted directly into the blood. 

Although the endocrine functions of the pancreas are critical to metabolic activities in the 

body, the endocrine portion of pancreas comprises only 1-2% of total pancreatic mass. 

The exocrine function of the pancreas is to produce and release potent enzymes to break 

down dietary protein and fat into molecules that can be absorbed by the GI tract. One 

hallmark of the exocrine pancreas is the production of zymogens, or proenzymes, that 

must be cleaved into an active form. The active form of these enzymes is far too potent 

to be stored within the pancreatic acini and therefore are secreted as zymogens into the 

duodenum where they are then activated. Trypsinogen and chymotrypsinogen are the 

two main zymogens. Enterokinase cleaves trypsinogen into trypsin and trypsin, in turn, 

cleaves chymotrypsinogen into chymotrypsin. Amylase and pancreatic lipase are 

secreted unchanged. Below is a table of the pancreatic enzymes, their function and 

stimulus for secretion. 

ŀ2012 DoveLewis Annual Conference 

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Enzyme Enzyme Function Stimulus Stimulus for for secretion 

secretion 

Trypsin Proteolytic 

Chymotrypsin Proteolytic 

Amylase 

Hydrolyzes CHO into 

dissacharide 

Hydrolyzes fat into fatty 

Pancreatic lipase 

acids 

Cholecystokinin 

Acetycholine 


Acetycholine 


Acetycholine 


Acetylcholine 

If the pancreas contains such highly destructive proteolytic enzymes why doesn’t the 

pancreas autodigest? There are innate protective mechanisms that prevent this from 

happening. Enterokinase is only located in the duodenum which prevents intra-ductal 

activation of enzymes. Pancreatic ductal cells secrete highly alkaline fluid. The HCO3- 

concentration is 5 times that of serum. Trypsin inhibitor enzyme is naturally found within 

the ducts that inactivates any trypsin that may be located within the ductal system. 

Lastly, there are circulating plasma anti-proteases such as α2 macroglobulin and α 

antitrypsin which act to neutralize active circulating enzymes. Knowing why the 

pancreas does not spontaneously autodigest is an easy answer. Knowing why these 

mechanisms fail is still unclear. The key is the intraductal activation of trypsin that then 

activates other enzymes resulting in pancreatic autodigestion. Circulating antiproteases 

likely become overwhelmed and are ineffective at stopping the process. Pancreatitis 

presents as a spectrum. Mild cases produce little inflammation and is self limiting. In 

acute or severe forms, the damage is not limited to the pancreas. Release of inflammatory 

mediators, vasoactive substances and oxygen free radicals can lead to hypotensive shock, 

multiorgan failure, DIC, and death. The remainder of this discussion will focus on the 

acute, severe presentation of pancreatitis. 

Clinical signs commonly noted include vomiting, anorexia, abdominal pain, and fever. 

This can be accompanied by varying degrees of shock. Uncommon but serious 

complications include coagulopathy, pleural effusion and multiorgan dysfunction. CBC 

may show mature neutrophilia with left shift +/- toxic change or possibly a degenerative 

left shift (bands and neutropenia) if the patient is septic. Chemistry profile can be 

variable. Azotemia can be pre-renal or renal if primary renal compromise has occurred 

secondary to prolonged hypoperfusion or microthrombi in the kidneys. Elevated liver 

enzymes can occur secondary to reactive hepatitis or sepsis. Low ionized calcium may be 

noted and is secondary to saponification, the process whereby fatty acids chelate calcium 

salts. Hyper- or hypoglycemia may be seen and amylase and lipase are generally very 

elevated. 

The inflammatory process is a fluid one. With severe cases of pancreatitis, or any disease 

where inflammation is the driving force, reassessment of organ function is critical to 

determining the progression of disease. Do not underestimate the risk of organ 

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dysfunction in a sick pancreatitis patient. We do not have a good sense of how many 

dogs with necrotizing pancreatitis have concurrent infection. Necrotic pancreatic tissue is 

theoretically a good substrate for ascending bacteria from the duodenum. But bacterial 

translocation from an ill gut is more likely to be a cause for sepsis in severe pancreatitis 

cases. 

In humans contrast enhanced CT is the gold standard for diagnosis of pancreatitis. CT is 

better able to identify areas of the pancreas that are necrotic or concurrent infected. This 

modality is rarely available for veterinary use. Abdominal ultrasound has 68% sensitivity 

in detecting pancreatitis – although this is largely operator dependent. Typically what is 

noted sonographically is a thickened, hypoechoic pancreas with hyperechoic 

peripancreatic fat. The duodenum usually appears atonic. Free fluid might also be 

present. Traditionally serum amylase and lipase have been used as markers for 

pancreatitis. The catalytic enzyme assay test for lipase measures lipase from all cellular 

sources and is not specific to the pancreas. The immunoreactivity assay offers a species 

specific test for pancreatic lipase. This assay involves purified canine pancreatic lipase 

and polyclonal anti-canine pancreatic lipase antibodies raised in rabbits. The canine 

specific pancreatic lipase immunoreactivity has 82% specificity. It does not differentiate 

between chronic and acute pancreatitis. Long term steroid therapy does not affect level. 

The sample should be a non-hemolyzed 12 hour fasted sample for best results. 

Causes of pancreatitis include intrinsic factors such as biliary disease, 

hypertriglyceridemia, gastric/duodenal disease, and primary pancreatic disease – tumor, 

cyst. Extrinsic factors include diet, drugs/toxins, and surgical manipulation. Drug 

associated pancreatitis is not fully understood. Direct effects could include direct toxicity 

or hypersenstivity reaction. Indirect effects could include ischemia, thrombosis, and 

increased viscosity of pancreatic fluid. Below are examples of drugs associated with 

pancreatitis in people. I chose ones that we commonly use in our veterinary patients. 

There have not been formal studies conducted on the effect of any of these drugs on the 

pancreas in canine except for L-spar. In a small cohort of dogs, L-spar did not elevate the 

CPLI levels in dogs with lymphoma. But there are case reports and anecdotal evidence to 

suggest that L-spar, azathioprine and steroids are associated with pancreatitis. 

• Asparaginase 

• Azathioprine 

• Cisplatin 

• Enalapril 

• Furosemide 

• Steroids 

• TMS 

• Tetracyclines 

There is a long held belief that there is a link between diet and pancreatitis. There are 

studies that support the correlation between high fat diet and the incidence of 

pancreatitis in dogs. But studies that support a direct cause and effect between high fat 

diet and onset of pancreatitis are lacking. Lem et al in 2008 published a retrospective 

study examining 198 dogs with pancreatitis and compared several parameters to 187 

dogs with renal failure without pancreatitis. Diet history, body condition score, surgical 

history, and bloodwork were all examined. Below is the summary of their findings. 


Risk Risk Factor Factor 

Odd Ratio for Development of of 

Pancreatitis 

Pancreatitis 

Table scraps ingestion 2.2 

Trash ingestion 13.2 

Overweight 2 

Diabetes 3.6 

Previous urgent surgery 27 

Miniature Schauzer or 

Yorkshire Terrier 

4.2 

The authors made a point to note these findings do not suggest causes of pancreatitis 

rather identify risk factors for development of pancreatitis. And it may be a convergence 

of different factors in any patient that causes pancreatitis. 

Treatment for acute pancreatitis is largely supportive with fluid therapy being a primary 

therapeutic focus. Fever, effusion, GI loss, and an increased metabolic rate put the 

patient at constant risk for hypovolemia. Gastroprotectants and antiemetics are routinely 

used. Generally an H 2 blocker or proton pump inhibitor combined with a centrally acting 

anti-emetic are effective. Analgesics are a mainstay of acute pancreatitis therapy as well. 

A partial agonist such as butorphanol generally has neither the duration of action nor the 

analgesic efficacy to make it a good choice for pancreatitis. Buprenorphine may be a good 

choice for those dogs sensitive to pure mu agonist or one that subjectively is not very 

painful. A pure mu agonist at a scheduled dose frequency or used as a continuous rate 

infusion is generally recommended at presentation for severe, acute cases. Don’t be 

afraid to get creative. Microdoses of ketamine, dexmedetomidine, and lidocaine can be 

useful adjunct drugs, especially when used as CRI. You’ll find useful drug doses in the 

handout. 

Many clinicians will use fresh frozen plasma working on the theory that FFP contains the 

anti-proteases that may help neutralize enzymes. Protease activity does not perpetuate 

clinical signs, thus inactivation has limited benefit for outcome. FFP also has antiinflammatory 

proteins such as albumin which could be beneficial. Thus far, retrospective 

studies examining the use of FFP in canines and humans with pancreatitis have not 

shown survival benefit. 

Antibiotic use in pancreatitis is another controversial therapy. In humans, antibiotics are 

only considered in patients with necrotizing pancreatitis. Remember a necrotic pancreas 

does not start off infected, it only becomes infected after a period of time. The question 

in human medicine has remained does the prophylactic use of antibiotics in necrotizing 

pancreatitis reduce the risk of infection of the pancreas. The question as well as the 

clinical studies have evolved over the last few decades. A recent review of 10 major metaanalyses 

regarding the use of prophylactic antibiotics in pancreatitis with necrosis 


showed no benefit in the reduction of infection or mortality. However when the 

carbapenem groups were stratified a marginal benefit was seen. Over 5000 patients were 

represented in these 10 randomized clinical trials. Most of these patients were diagnosed 

with pancreatic necrosis via CT. Only 2/10 studies showed reduced mortality, 3/10 

showed reduced pancreatic infection, and 1/9 showed reduced need for surgery. 

Unfortunately clinical information is scarce on the use of antibiotics in canine pancreatitis. 

Furthermore, studies indicate the pharmacokinetics of drugs change in inflamed organs. 

For example Trudel et al in 1994 showed clindamycin, choramphenicol, metronidazole, 

and ciprofloxacin all achieve therapeutic levels in inflamed canine pancreas, where 

ampicillin did not. With this information routine use of antibiotics in acute pancreatitis is 

not recommended. However a worsening of the patient’s status and markers for sepsis 

would warrant reconsideration. 

Surgical intervention in pancreatitis is not commonly warranted. Certain disease 

processes such as pancreatic tumor or abscess would be surgical conditions. Necrotizing 

pancreatitis itself would not necessarily be an indication for surgery, however if the 

patient is not responding to medical therapy then surgical exploration should be 

considered. There is no accepted timeframe or recommendation when to make this 

decision. In the absence of definitive surgical indication, the decision to go to surgery 

based on the severity of condition, poor response to therapy or documented worsening 

during therapy. 

There is a JVECCS 2009 retrospective study of dogs that under went surgical 

management for pancreatitis. Reasons to proceed to surgery included abscessation, 

necrosis, biliary obstruction, and mass effect. The overall survival was 63%. 

Complications included intraop and post-op hemorrhage 12 dogs, Post-op development of 

diabetes 3 dogs, EPI 1 dog, and Septic abdomen 2 dogs. Their conclusions were to set 

specific parameters to determine when surgical intervention would 

The approach to nutrition in severe pancreatitis has traditionally been to keep the patient 

NPO for several days. This was based on the notion that enteral feeding stimulates 

pancreatic enzyme activity and total pancreatic rest did make sense. But let us consider 

the consequences of oral malnutrition. Enterocyte atrophy can occur in as little as 72 

hours with complete recovery occurring in 3-5 days. Unlike most other cells, the microvilli 

get most of their nutrition directly from nutrients passing by in the lumen of the gut, not 

through the blood supply, meaning even if patients are getting nutrition parenterally, 

enterocyte atrophy can still occur. The gut is also the site of gut-associated lymphatic 

tissue which is responsible for systemic and local GI immunity. In the starved gut there 

is loss of villi, flattening of vili, loss of tight junctions between epithelial cells, atrophy of 

GALT tissue, and decreased secretory immunoglobulins to the surface of the intestinal 

mucosa. Loss of villi makes reintroduction of nutrition more difficult. And a decreased 

gut mucosal barrier and immune function increases the risk for bacterial translocation 

and sepsis. 

Illness also accelerates metabolic consequences of starvation such as increased protein 

utilization, decreased protein production and increased metabolic rate. So the benefits of 

early nutritional intervention could help decrease these effects and protect against 

bacterial translocation. The basis for keeping patients NPO during pancreatitis stands on 

the assumptions that pre-jejunal feeding stimulates pancreatic enzyme secretion and that 

pancreatic enzyme secretion is what perpetuates clinical disease. It has been 

demonstrated that oral feeding stimulates pancreatic enzyme secretion more than post 

duodenal feeding. However it also has been shown recently that the inflamed pancreas is 


less responsive compared to the healthy pancreas – opening the door for the possibility 

that oral feeding may not be as detrimental as once thought. 

Numerous retrospective studies have demonstrated the benefit of post duodenal feeding 

compared to parenteral feeding and NPO. However there are no prospective randomized 

clinical trials comparing enteral feeding (oral or jejunal) to NPO. There have been a few 

pilot studies with small groups of people (20-50) comparing oral to jejunal feeding which 

are promising and may lead to larger clinical trials. A small pilot study was recently 

performed in 10 dogs with severe acute pancreatitis. They were randomized to either 

receive parenteral nutrition (NPO) or enteral nutrition. Although it was not adequately 

powered to prove significance, there were fewer complications and fewer incidences of 

vomiting in the enteral nutrition group. The take home message from these studies is 

that we should rethink the idea of keeping patients NPO for prolonged periods of time. A 

practical approach might be to consider keeping a patient NPO for 12 – 24 hours and feed 

if vomiting is minimal. We must also consider the length of time prior to admission that 

the pet has been anorexic. Parenteral nutrition or jejunostomy tube should be considered 

if anorexia prior to admission has been more than 2 days or if the patient is very 

intolerant to enteral feeding. 

Pancreatitis is a potentially devastating disease process that presents as a spectrum in 

canines. The most severe form is the acute onset pancreatitis with necrosis. This disease 

is largely one of medical management. Although much has been discovered regarding the 

proper approach to treatment of the pancreatitis patient, there are still unknown and 

unproven therapies. Considerations include fluid therapy, gastroprotectants, pain 

management, nutritional intervention and monitoring for development of multiorgan 

dysfunction. 

DRUG DOSE CRI 

Morphine 0.5 – 1mg/kg IM/SQ q 4-6hr 0.1 – 0.2 mg/kg/hr 

Fentanyl 3 – 8 mcg/kg/hr 

Hydromorphone, 

0.05 – 0.2 mg/kg IV q4-6 hr 0.01 – 0.03 mg/kg/hr 

Oxymorphone 

Buprenorphine 0.005 – 0.02 mg/kg IV q8 hr 

Tramadol 2-5 mg/kg PO q6 – 12 hr 

Dexmedetomidine 1-5 mcg/kg/hr 

Ketamine 5 – 20 mcg/kg/min

Canine Acute Pancreatitis Ladan Mohammad-Zadeh ... - DoveLewis

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