Beaner Has Exocrine Pancreatic Insufficiency: Beaner"s Story (Part II)

Beaner’s story is shared by Angie Falcsik of  Pawsitive K-9 Obedience. You can also follow her on Twitter or Facebook. If you haven’t yet, don’t forget to read the first part of the story first.

Check out my earlier article to learn more about Exocrine Pancreatic Insufficiency and what pancreas does.

Everything Beaner ate was going right through her and that she was likely suffering from EPI; Exocrine Pancreatic Insufficiency.

I said, “exocrine, what?” The vet explained that there are certain cells (acinar cells) found in the pancreas that are needed to produce and secrete enzymes needed to digest food. They are:

1. Amylase for digestion of carbohydrates (sugars & starches in grains, fruits & vegetables);


2. Lipases for digestion of fats and oils; and,


3. Trypsin and Proteases for digestion of proteins.

Beaner can no longer produce what is necessary to digest her food and allow her body to absorb and utilize the nutrients – basically, she was literally starving and without treatment, would not live!  

EPI is not curable, only treatable with specific enzymes. I made another appointment to go in as soon as the other tests were completed.

After hanging up with the vet, I sat down and cried!  

How could I not have known it was this serious? What kind of mom am I?  Why didn’t I take her in sooner?  I decided to do some research.  I read more about the enzymes that were needed to digest food, about how this disease can affect other parts of a dog’s body; organs, immune, nervous system, and mental status. Dogs suffering from exocrine pancreatic insufficiency can become depressed, aggressive and/or fearful.

I also found out that this disease is very hard to diagnose and that many times the obvious symptoms do not reveal themselves until 80-90% of the exocrine pancreas acinar cells are destroyed.  

While that did not change anything, it at least eased my mind a little in that I was not beating myself up – as much. I pride myself on being very aware of my dog’s health and daily routines and now this is the second dog that something serious has happened and I didn’t realize it immediately. First Indy with his dysplasia and now Beaner with EPI.

A few days later we were back at the vet.

Beaner’s urine test was perfect and her blood work was as well. No protein loss and no cancer.  

The vet discussed a more specific test where blood would be drawn again and sent down to Texas, the only lab in the US that conducts this particular test and runs approximately $ 200.00. This test, called a cTLI test, is the only test that can confirm EPI. One is looking for a range between 5.0-35.0.

Now I had to decide what to do.

Her blood work was normal, her urine was normal, her stool was grey, slimy, running, she was loosing weight, bony frame, losing hair, fur turning brittle, mental status changes, tummy gurgling/gas – classic EPI symptoms. The enzymes she would be started on is $ 150.00 a bottle which lasts approximately 6-8 weeks.

I made the decision to start Beaner on the pancreatic enzymes without having the cTLI test as I completely trust my vet and he has seen this many times before and has patients suffering from this disease.  

Of course, we could perform the cTLI at any time if I chose to do so but for now, I chose to get her started on the enzymes right away.

There are a few ways of treating this, but the recommended treatment is powdered porcine pancreatic enzyme, which, by the way, does not smell very good.  

The vet warned me it smells like vomit and I asked if Beaner will even eat it if it smells that bad. His response, “she eats poo doesn’t she?”.

Touché. As it turns out, it is not as bad as they made it out, but you definitely do not want to get your nose too close!  I picked up a few cans of pumpkin and canned dog food on our way home with enzymes in tote.

The directions state that the enzymes must “incubate” for a minimum of 10-15 mts so I measured 1 tsp with a good size spoonful of canned food, mixed it really well and let it sit for the appropriate time. Meanwhile, the dogs are going crazy because they know it’s dinner time, they see me preparing the food and then they have to wait! Not happy campers I tell you! 

I continued this regimen for a few days.

I got Beaner’s food ready in the morning after my work out and while I was getting ready for work which worked out well, but it was the dinner time regimen that was a nightmare for everyone.

I remembered a Yahoo Group that I found and joined for owners of EPI dogs and posted my dilemma. 

I received a number of really great responses! Many people had to same situation I did. They worked late, multiple jobs and didn’t want their dogs to have to wait to eat after a long day.

It was also recommended that depending on the level of the disease, feeding small amounts multiple times a day was the best thing to do until it was under control.

The idea that worked best for me was place her dry kibble in containers along with the enzymes and shake really well so all the kibble is coated. I have about 5-6 containers in the fridge at all times. When I feed the dogs at night, I add just enough water to barely coat the kibble and let it sit over night for her morning feeding.  In the morning, I do the same thing for her evening feed.

This is a great idea if one is going on vacation and either has a pet sitter coming in or wants to make sure the boarding facility has the appropriately mixed food/meds.  It was even suggested to mix food, meds and meds, let it incubate a few hours and then freeze it! 

With my schedule, working 3 jobs, and crazy hours, this formula works great for Beaner.  If I’m going to be running late, I can have a neighbor come over and feed the dogs and know she is getting exactly what she needs.

Okay, so back to our story.

The first week was difficult as I was not seeing any changes in her behavior, appetite, poo eating regimen, attitude, weight – nothing!  

I called the vet and he said we needed to give it a bit more time. If I was still not seeing any changes in another 4-5 days, we would move forward with cTLI test.

A few days later I was looking out the window and saw Indy outside doing his duty and Beaner right next to him waiting for him to finish. I was just about to tell her to leave it so I could pick it up when much to my surprise, she sniffed it and walked away!  I knew that this meant progress was occurring and she was feeling better!  The enzymes were working!

Each day I noticed more and more signs that she was doing better.  

She was not as ravenous at the food bowl, her fur started to feel less brittle and after about a week, actually started feeling soft again! She began to get that spark back in her eyes and spunk in her attitude!  She even began to smile and wink at me again!

She was able to play and walk longer without getting so tired she could barely stand up and her mental status became more stable.  

She became tolerant of the little things again and her depression was going away. I knew she was really feeling better when her nosework started going from hunting for the food box because she was starving to hunting because she loved the game!  My girl was back!

It has now been about almost a month and she has gained 5 pounds!  

Her fur is really soft again, she plays, throws her toys at me, runs and has that sparkle in her eyes again!  We still have a ways to go to put another 12-15 pounds but we are well on our way to better health.  Although her normal weight when she was younger and healthier (developing some hip/joint issues), the vet and I decided not to bring her weight back to her 76-80 pound weight but to keep her at about 70-72 so as not to put too much pressure on her joints. 

Beaner will need to have her enzymes for the rest of her life, but now that we have finally gotten the right diagnosis, she is getting healthier day by day!  

I do of course, continue to read and converse with my Yahoo EPI group as  there is always something that comes up in someone’s life that we can learn from to help Beaner in her recovery. They have been a wonderful support group and wealth of information.

***

For nearly 10 years, Angie Falcsik has been professionally dedicated to the training, rehabilitation, and rescue of dogs. But the roles of trainer, rescuer, and rehabilitator have been a large part of her life since she was a child. Angie’s life-long passion and the goal of her professional career is to educate people regarding responsible dog ownership and the realities involved in being a responsible dog owner. Angie has been working with Animal Control agencies and shelters for many years and has offered expert advice and testimony in animal abuse and neglect cases. Angie has been professionally training dogs since 2002 and is an AKC Canine Good Citizen Evaluator. Through her classes, private in-home training, and rescue work, she has trained hundreds of dogs. In her own home alone, she has fostered and trained over 350 dogs!

Angie’s unique obedience class (Language and Leadership) focuses on pack leadership, body language, and positive reinforcement. Her classes involve training the owner and family members and rehabilitating the dog. Angie’s method uses body language as well as voice commands to develop and establish an appropriate relationship between owner and dog. If your dog is not listening to you, chances are, your dog does not have sufficient respect for you. Angie will teach you how to become a pack leader and earn the necessary respect so that following your lead becomes second nature to your dog.

In Angie’s class, you will learn the importance of pack leadership, establishing rules and boundaries, along with an exercise regimen, and how to implement these essential aspects of responsible dog ownership into your lives. You and your dog will also learn basic obedience such as heel, sit, wait, down, and come, as well as additional training/rehabilitation measures that are specific to your dog and family. While some basic training is essential for all dogs, Angie believes that not every technique works or is appropriate for every dog and family. Each dog and family is unique and Angie’s training philosophy and methods are designed to address and work with different family/dog situations and living styles.

Related articles:
Weight Loss, Brittle Fur, Starving All The Time … Beaner’s Story (Part I)
Exocrine Pancreatic Insufficiency (Maldigestion)


Further reading:
Exocrine Pancreatic Insufficiency (Maldigestion Disorder) in Dogs
Exocrine Pancreatic Insufficiency at Veterinary Partner
EPI – Exocrine Pancreatic Insufficiency
Exocrine Pancreatic Insufficiency Forum for dog owners

Pancreatitis in Cats & Dogs Part 1: Introduction, causes, symptoms & diagnosis

The pancreas (image) is an organ in the body located next to the small intestine just after the stomach. It has two primary functions. It is an integral part of the digestion of food and it is the primary organ responsible for regulation of blood sugar in the body. When the pancreas is diseased, it can result in a very painful and debilitating condition called acute pancreatitis (Image). Disease of the pancreas may also cause diabetes mellitus (sugar diabetes) or chronic pancreatic insufficiency, EPI. (Image) EPI results in the inability of the body to digest foods properly. Pancreatitis has been documented in dogs for many years. Until recently it was not thought to exist in cats. We are now recognizing this disease more frequently in cats due to better diagnostic aids.
A recent study has shown that acute pancreatitis. is almost as frequent in cats as dogs. Chronic forms are more common than acute forms. Pancreatic insufficiency and pancreatic cancer are less common than inflammatory disease. Other forms of pancreatic disease in cats are cysts and pancreatic parasites.
Pancreatitis is inflammation of the pancreas resulting from auto digestion by prematurely activated zymogens.(1) It is the most common disorder of the canine exocrine pancreas and is being diagnosed more frequently in cats as awareness increases and diagnostic tools improve.(1,2) The disease can be classified as acute (reversible following removal of inciting cause) or chronic (irreversible changes from on-going inflammation), and mild or moderate to severe.(1) Cats tend to have more of a chronic disease than dogs.(2) The diagnosis of pancreatitis is usually presumptive, as pancreatic biopsy is not always an option. Although several diagnostic tests have been advocated for use in the diagnosis of pancreatitis, many of them are not sensitive enough to be clinically useful.
The main causes of acute pancreatitis may be caused from an on-going or long-term viral infection, poor diet, stress and from certain medications. Symptoms of acute pancreatitis are similar to chronic pancreatitis. Symptoms of chronic pancreatitis can include, but are not limited to moderate to severe abdominal pain, nausea, fever, reduced mental acuteness, abdominal swelling, weight loss and fatty stools. Symptoms of an acute pancreatitis or inflammation are abdominal pain, nausea, vomiting, weakness, anxiety, fever, abdominal gaseous fullness, abdominal indigestion, chills, fatty stools, anxiety and weight loss.
The Merck Veterinary Manual defines as causes of the disease: “Pancreatitis in dogs can be caused by a high fatty diet, eating a large fatty meal at one sitting, obesity, an underlying condition, some medications, and genetics. For example, some dogs that are fed pork products or dark chocolate develop pancreatitis as a result of the sudden amount of fats that enter the body. In some cases the cause of pancreatitis is termed ‘idiopathic’ meaning the cause of the condition remains unknown.”
Dr. Laura West, D.V.M. and Dr. Frederic Almy, D.V.M. write in their abstract “Diagnosing Pancreatitis in Dogs and Cats by Laboratory Methods”: “The underlying cause of most cases of pancreatitis is usually unknown in both dogs and cats; however, there is a considerable list of associated risk factors. Obese animals as well as animals fed a diet high in fat are more prone to developing pancreatitis.(1,3) Hyperlipidemia has been associated with pancreatitis, although it is unclear whether it is a result of the pancreatitis or part of the cause. Certain breeds of dogs are considered predisposed to developing pancreatitis, such as the miniature schnauzer or terrier breeds.(1,3) A large number of drugs and drug classes have been thought to cause pancreatitis in people, but a direct causal relationship has not been established. Drugs used in veterinary medicine that may be associated with pancreatitis are numerous and include L-asparaginase, azathioprine, estrogen, furosemide, potassium bromide, salicylates, sulfonamides, tetracyclines, thiazide diuretics and vinca alkaloids, among others.(1,3)
Additional causes or risk factors for pancreatitis include exposure to scorpion venom, zinc toxicosis, hypercalcemia, congenital anomalies of the pancreatic duct system, reflux from the duodenum into pancreatic ducts (secondary to surgical creation of a closed duodenal loop, blunt trauma, or vomiting), surgical manipulation (rare), pancreatic ischemia and endocrinopathies (hypothyroidism, diabetes mellitus, hyperadrenocorticism).(1,3)
In cats, toxoplasma gondii and Amphimerus pseudofelineus (hepatic fluke) have an established causal relationship with pancreatitis. Feline infectious peritonitis and panleukopenia have also been implicated. As in the dog, blunt trauma, surgical manipulation and ischemia can result in pancreatitis. Organophosphate intoxication and inflammatory diseases of the liver and intestines are also implicated as causes.(2,3)
In the normal pancreas, proteolytic and phospholipolytic enzymes are synthesized, stored and secreted as inactive zymogens and it is these enzymes that are utilized in the majority of diagnostic tests for pancreatitis. The pancreatic zymogens are only activated once they are cleaved, a process which does not normally occur until they reach the small intestine. Once in the small intestine, enteropeptidases from duodenal enterocytes cleave trypsinogen to make trypsin, which can then activate other zymogens.(1)
Pancreatitis is the end result of a cascade of events but is ultimately caused by the autodigestion of the pancreas.(4) Current literature suggests that this cascade of events begins with a decrease in secretion of pancreatic enzymes in response to some noxious stimulus.(4) Subsequent to the decreased secretory activity, abnormal fusion of lysosomes and zymogen granules results in premature, intrapancreatic activation of trypsinogen.(1,4)
When premature activation of trypsinogen occurs, there are mechanisms in place which limit the activation of other zymogens. First, trypsin is very effective at hydrolyzing itself. Second, pancreatic secretory trypsin inhibitor is synthesized, stored and secreted with the digestive enzymes. If significant activation of trypsin occurs within the acinar cell or duct system, this molecule will inhibit trypsin activity. Additionally, α-macroglobulin and α1-proteinase inhibitor are protease inhibitors in the plasma.1 However, once inhibitory mechanisms are overwhelmed, more zymogens become activated, inflammatory mediators and free radicals are released, and pancreatitis develops.(1)
Common clinical signs in dogs with acute pancreatitis include anorexia (91%), vomiting (90%), weakness (79%), and abdominal pain (58%).(1,5) Abdominal palpation may reveal a cranial abdominal mass.(1,3) A retrospective study of 70 cases of acute canine pancreatitis reported dehydration in 97%, icterus in 26%, fever in 32%, abdominal pain in 58%, and obesity in 43% of dogs at the time of initial examination.(5) Other systemic complications can include respiratory distress, bleeding disorders and cardiac arrhythmias.(1,3)
On the other hand, cats have extremely variable histories and clinical signs. More typical clinical signs include anorexia (97%), lethargy (100%), and dehydration (92%).(6) Vomiting and abdominal pain, while common in the dog, are less frequently reported in the cat (35% and 25%, respectively).(6) Other clinical signs reported include hypothermia, dyspnea, diarrhea, ataxia, and weight loss.(6) Pancreatitis in cats has a tendency to occur with certain other diseases, such as cholangiohepatitis/cholestasis, nephritis, diabetes mellitus, and inflammation or ulceration of the intestines.(2,3)
The cause for acute pancreatitis in most cases is not known. Several cases have been reported that were caused by trauma, abscessation of the pancreas, ingestion of certain food borne toxins, and of pancreatic duct obstruction. In cats, infectious agents such as toxoplasma, herpes virus, FIP, and feline parvo virus may cause pancreatitis. Some cases of liver disease may also cause pancreatitis, such as cholangiohepatitis and fatty liver disease in cats. Clinical signs are non-specific. Fever, rapid heart rate and vomiting, abdominal pain were observed as well as lethargy loss of appetite, and dehydration. Other signs include respiratory distress, and icterus (jaundice). Diagnosis is made by history, clinical signs, x-ray and ultrasonography. The latter is most helpful in the diagnosis. A blood test called the trypsin-like immunoreactivity (TLI) has been very helpful in the diagnosis of the disease. High blood sugar levels are also common with the disease in cats and some cats become diabetic following recovery from acute episodes of pancreatitis. Newer tests are now available, but the tests are still not one hundred percent reliable. Most of the diagnostics are performed by clinical signs. Ultrasound is proving to be invaluable in the process of ruling out other diseases.
The most common cause of pancreatic insufficiency is chronic pancreatitis. With chronic pancreatitis there is an absence of digestive enzymes. Therefore, food will pass through the digestive tract without being absorbed. Thus, a form of malabsorbtion of food occurs. This form of pancreatitis in cats is commonly accompanied by diabetes since both the digestive as well as the insulin producing cells of the pancreas are involved. Clinical signs of chronic pancreatitis include soft, pale and voluminous stools, weight loss, greasy soiling of the area around the rectum, and sometimes the entire hair coat.
Note: Treatment of animals should only be performed by a licensed veterinarian.
Sources:
Merck Veterinary Manual
Laura D. West, DVM and Frederic S. Almy, DVM, MS, Diplomate ACVP
VCA Columbia Animal Hospital
Images: Hill’s pet Food
References
1. Williams DA, Steiner JM. Canine Exocrine Pancreatic Disease. In Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine, Diseases of the Dog and Cat, 6th ed. St. Louis, Elsevier Saunders, 2005, pp. 1482-1487.
2. Steiner JM, Williams DA. Feline Exocrine Pancreatic Disease. In Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine, Diseases of the Dog and Cat, 6th ed. St. Louis, Elsevier Saunders, 2005, pp. 1489- 1491.
3. Simpson, KW. Diseases of the Pancreas. In Tams T. (ed): Handbook of Small Animal Gastroenterology, 2nd ed. St. Louis, W. B. Saunders Co, 2003, pp. 353-365.
4. Steiner JM. Diagnosis of acute pancreatitis. Vet Clin North Am Small Anim Pract 2003; 33: 1181-1195.
5. Hess RS, Saunders HM, Van Winkle TJ, et al. Clinical, clinicopathologic, radiographic, and ultrasonographic abnormalities in dogs with acute pancreatitis: 70 cases (1986-1995). J Am Vet Med Assoc 1998 Sep1; 213(5): 665-70.
6. Hill RC, Van Winkle TJ. Acute necrotizing pancreatitis and acute suppurative pancreatitis in the cat. A retrospective study of 40 cases (1976-1989). J Vet Intern Med 1993; 7: 25-33.