Revised December 2011.
Commonly called bloat, sometimes described as gastric dilation/volvulus (GDV), this is a terrifying and usually fatal emergency disorder that German Shepherds and many other deep chested dogs experience. A twisting of the entrance and exit to the stomach traps the food and gas. As the stomach swells, the twist is more unlikely to be relieved without veterinary help. Great strides in surgical treatment have been made, but the key to reducing the high mortality is still time. Recognize the symptoms and get the dog to a veterinary surgeon, preferably an emergency or trauma-oriented hospital. Simple dilation (swelling due to gas) may not be serious as long as the dog is able to pass food into the duodenum, but it has been estimated that 80 percent of all dogs that experience simple dilation will someday also have torsion.
Symptoms of torsion include a swollen, turgid abdomen; the sluggish action of the dog; his white, frothy, unsuccessful attempts at vomiting; and perhaps his scratching in the dirt to make a cool hole in which to lie down. Also, the spleen will feel like a hard lump. This organ is normally wrapped around some of the stomach and therefore splenic torsion usually accompanies gastric torsion, and sometimes occurs without stomach torsion. When either happens, the return of the blood that flows through the spleen is shut off, causing shock, the “immediate” killer.
The first thing your vet is likely to do is attempt to push a tube down the throat into the stomach so the gas pressure can be relieved. If he cannot get past the twisted part of the alimentary canal, he may opt for immediate surgery so he can untwist the organs. One emergency veterinary service in the Detroit area uses a different kind of lavage tube in their treatment of acute torsion. The large diameter, stiff, black polyethylene pipe has a smaller, flexible tube inserted into it. This smaller tube is for warm water so that the stomach contents can be flushed out of the larger one for about fifteen minutes. In either case, once the dog has been stabilized, decisions can be made about whether to operate, or untwist a stomach or spleen still in volvulus.
Follow up surgical techniques are numerous, but perhaps the one with the most success in preventing future torsion is a tube gastrostomy. In this procedure, a rubber or vinyl tube is put into the stomach through the abdominal wall, and in a week the stomach wall at that point becomes attached with scar tissue to the peritoneum and abdominal wall. The tube is then pulled out. The surgical opening seals off in a few days, and since the stomach is fused to the abdominal wall, it is prevented from again twisting out of position. Regular gastroplexy, which is suturing the stomach to the abdominal cavity, is also widely performed. Because of these and other techniques, especially the rise of emergency clinics, the mortality rates among those that make it to the clinic while still alive has plummeted to about 15 percent. Another 15 percent or so die without being seen by the vet first.
Groups of scientists at many locations have been studying bloat for a long time, partly with help from such as Morris Animal Foundation, the GSDCA, and many others. So far, they have identified a number of likely causative factors, including behavioral traits. Breed susceptibility is pretty obvious, with 25 percent or more of Great Danes, Saint Bernards, Weimaraners, and Irish Setters expected to suffer from bloat sometime during their lives. German Shepherd Dogs, Standard Poodles, Collies, and Gordon Setters are fairly high on the incidence lists, also. Some of the characteristics seen most often in dogs that had bloated include some stressful event, even minor, in approximately the eight hours prior to the incident, a fearful temperament, and consumption of fairly large quantities of non-food material. The only dogs I’ve had direct contact with that bloated were of impeccable character, but those may have been in the minority. Purdue researchers found no pattern in presoaking dry food or not, but a slight correlation between several smaller meals and less bloat. Others found no relation to soybean meal, an early target of breeders looking for a primary cause in the food. In fact, unsubstantiated rumors about the supposed connection between bloat (GDV) and soybean meal in the dog food caused manufacturers to drop that ingredient. It has definite benefits to human health, and perhaps it is unfortunate that our dogs are not getting any of it now. Adding vegetables and canned or meat scraps to a basic grain-based commercial feed appears to help lower incidence. Most dogs (60%) bloated, not immediately after vigorous exercise soon after a meal, but in mid- to late evening when resting or sleeping.
Less likely are other types of torsion, but they can be as life-threatening. Splenic torsion can occur without gastric twisting, and an even more rare disorder is mesenteric root torsion. The mesentery is the white, fibrous, web-like or film-like tissue that connects the various sections of intestines to each other and to the abdominal wall. Blood vessels travel through the mesentery, and if there is a twisting there, regardless of whether the intestine itself is closed off, the blood supply can be halted and the intestinal tissue can become necrotic. Bloody diarrhea, vomiting, abdominal swelling and/or pain, and shock or general collapse can be symptomatic. It may be the same as what some call “twisted intestines”. So few dogs survive that it is impossible to prevent recurrence or conclusively predict whether those are at greater risk for another attack than any other dog is.
There is a familial element in torsion/volvulus in many, similar to the way cancer “runs in families”, but most cases don’t give much of a clue to hereditary factors. As in “toxic gut syndrome” which is also seen a lot in some GSD lines, it is almost impossible to tell which came first, the presence of abnormal bacterial populations and irritated intestinal or stomach linings, or the bloat itself. Which is cause and which is effect is not going to be easy or even possible to determine. Some investigators suspect that breeders may be stuffing their small, young puppies’ stomachs too much, with results that show up only later in life. Work goes on. Dr. Larry Glickman and his group at Purdue University as well as others have published several papers on this syndrome. Dr. Glickman commented that the supposed claim that raised food bowls are correlated with increased incidence in torsion/bloat may just mean that this allows a dog to swallow more food (and air?) more quickly than if they were on the floor. A couple of website references such as had some info, including from JAVMA’s Nov 15, 2000 issue. An abstract follows:
Canine Gastric Dilatation-Volvulus (Bloat) School of Veterinary Medicine, Purdue University, West Lafayette, IN
Non-dietary risk factors for gastric dilatation-volvulus in large and giant breed dogs. Lawrence Glickman, VMD, DrPH; N.W. Glickman, MS, MPH; D.B. Schellenberg, MS; M. Raghavan, DVM, MS; T. Lee, BA
Summary of findings: (references 1 & 2) A 5-year prospective study was conducted to determine the incidence and non-dietary risk factors for gastric dilatation-volvulus (GDV) in 11 large- and giant-breed dogs and to assess current recommendations to prevent GDV. During the study, 21 (2.4%) and 20 (2.7%) of the large and giant breed dogs, respectively, had at least 1 episode of GDV per year of observation and 29.6% of these dogs died. Increasing age, increasing thorax depth/width ratio, having a first degree relative with a history of GDV, a faster speed of eating, and using a raised feed bowl, were associated with an increased incidence of GDV. The table below summarizes the magnitude and direction of GDV risk associated with having each of these factors. The relative risk (RR) indicates the likelihood of developing the disease in the exposed group (risk factor present) relative to those who are not exposed (risk factor absent). For example, a dog with a first degree relative with a history of GDV is 1.63 times (63%) more likely to develop GDV than a dog without a history of GDV. As another example, if dog ‘A’ is a year older than dog ‘B’, then dog ‘A’ is 1.20 times (20%) more likely to develop GDV than dog ‘B’.
- Risk Factor – Relative Risk Interpretation
- Age: increase in risk for each year increase in age
- Chest depth: Increase in risk for each unit increase in chest depth/width ratio
- Considerable increase in risk associated with having a first-degree relative with GDV
- Raised food bowl: increase in risk associated with using a raised food bowl, contrary to popular opinion*
- Speed of eating [for Large dogs only]: increase in risk for each unit increase in speed-of-eating score
*Studies may be ongoing to clear up this concept.
Most of the popular methods currently recommended to prevent GDV did not appear to be effective, and one of these, raising the feed bowl, may actually be detrimental in the breeds studied. In order to decrease the incidence of GDV, we suggest that dogs having a first degree relative with a history of GDV should not be bred. Prophylactic gastroplexy appears indicated for breeds at the highest risk of GDV, such as the Great Dane. [Gastroplexy is a procedure that by surgery and scar tissue formation affixes various surfaces to each other to reduce chance of twisting.]
OBJECTIVE: To identify non-dietary risk factors for gastric dilatation-volvulus (GDV) in large breed and giant breed dogs.
DESIGN: Prospective cohort study.
ANIMALS: 1,637 dogs 6 months or older, of the following breeds: Akita, Bloodhound, Collie, Great Dane, Irish Setter, Irish Wolfhound, Newfoundland, Rottweiler, Saint Bernard, Standard Poodle, and Weimaraner.
PROCEDURE: Owners of dogs that did not have a history of GDV were recruited at dog shows, and the dog’s length and height and the depth and width of its thorax and abdomen were measured. Information concerning the dog’s medical history, genetic background, personality, and diet was obtained from the owners, and owners were contacted by mail and telephone at approximately 1-year intervals to determine whether dogs had developed GDV or died. Incidence of GDV, calculated on the basis of dog-years at risk for dogs that were or were not exposed to potential risk factors, was used to calculate the relative risk of GDV.
RESULTS AND CLINICAL RELEVANCE: Cumulative incidence of GDV during the study was 6% for large breed and giant breed dogs. Factors significantly associated with an increased risk of GDV were increasing age, having a first-degree relative with a history of GDV, having a faster speed of eating, and having a raised feeding bowl. Approximately 20 and 52% of cases of GDV among the large breed and giant breed dogs, respectively, were attributed to having a raised feed bowl. [end of abstract]
Another article based on the same research but with slightly different data pulled out for the particular subject matter, was published in 1997: Multiple risk factors for the gastric dilatation-volvulus syndrome in dogs: a practitioner/owner case-control study (by): Glickman LT, Glickman NW, Schellenberg DB, Simpson K, Lantz GC. JAAHA, May-Jun., 1997. ABSTRACT: A study was conducted of 101 dogs (i.e., case dogs) that had acute episodes of gastric dilatation-volvulus (GDV) and 101 dogs (i.e., control dogs) with non-GDV-related problems. The control dogs were matched individually to case dogs by breed or size, and age. Predisposing factors that significantly (p less than 0.10) increased a dog’s risk of GDV were: male gender, being underweight, eating one meal daily, eating rapidly, and a fearful temperament. Predisposing factors that decreased the risk of GDV significantly were a “happy” temperament and inclusion of table foods in a usual diet consisting primarily of dry dog food. The only factor that appeared to precipitate an acute episode of GDV [in their observations] was stress.
This contradicted the early-1990s study that indicated the opposite: that raised bowls should reduce the incidence of torsion/bloat. An article in “Bloat News” indicated a possible link that raised feeders might help prevent future episodes in a dog susceptible to “aerophagic” bloat (linked to swallowing too much air with the food, a commonly blamed cause at the time. Another issue of the same periodical indicated the single highest correlating factor was morphology (body type). A graph showed a sharp incidence increase as the depth of the chest exceeded its width and a strong correlation with body condition and temperament (weak nerves vs. calm, unstressed dogs). It may be good to select dogs that have strong, calm nerves, and are not slab-sided!
An article on the Foster and Smith Pet Education site, “Interpret Findings of a New Study on Bloat (Gastric Dilatation/Volvulus – GDV) with Caution”, December 2000, at: , starting with a subheading, “The Question of Raised Food Bowls” circulated among fanciers. An excerpt: “In this study, when analyzing the association between the rate of GDV and the height of the food bowl, some questions arise. First, the study found that large breed dogs whose food bowls are not elevated have the lowest risk of GDV. A confusing finding is that large breed dogs who have their bowl raised more than 1 foot have the next lowest risk, and those who have their food bowl raised somewhere between the floor and one foot have the highest risk. So, the risk of GDV is not proportional to the height of the food bowl. If height of the food bowl is important, why doesn’t the risk steadily increase, the higher the food bowl is raised? Secondly, it appears that the researchers did not consider the height of the animal in relationship to the height of the bowl when looking for an association between food bowl height and prevalence of GDV. It would be of interest to compare the height of the bowl to the height of the dog, since dogs in this study varied widely in height due to breed differences and age (some were only 6 months old).
“The third question is, ‘Why weren’t similar findings obtained in giant breed dogs?’ In giant breeds, dogs with food bowls raised less than one foot had the same incidence of GDV as those dogs who did not have their dishes raised at all. Finally, it is unclear if the researchers also analyzed whether the elevated feeders were being used because other medical problems were present or if the elevated feeders could influence other factors such as the speed of eating. Could these medical problems or other factors, rather than the elevated feeders, have contributed to the increase in GDV in this group? A second subheading was ‘Comparison to Other Studies’. The results of this study agree with most previous studies, which also found that GDV increases with age. On the other hand, in several studies, dogs who ate faster had higher rates of GDV. In this study, we had a peculiar finding: eating at a fast rate was associated with an increased rate of GDV in large breed dogs, but a decreased rate in giant breed dogs. There have been other contradictory findings in research on GDV. In some studies it was found that overweight dogs had higher rates of GDV, and in other studies, lean dogs had higher rates. In this study, weight did not seem to make a difference. In most studies, including this one, the rate of GDV between males and females were similar; in one study, however, males had an appreciably higher rate.”
One other item that was brought to light on a “VetMed” e-mail discussion list, was that there is no proven advantage to raised feeders, and that the Foster and Smith company (which runs the Pet Education website) sells many types of elevated feeders.
While some excellent work on GDV has been carried out at Purdue, some feel that very insufficient research has been done in the US on canine torsion/volvulus. Here are websites I was told will give information on GDV; I have not checked these out, so I cannot verify their usefulness. Some may be “foreign links, as well as human links and livestock links” as the person who gave me this list said. Since website addresses frequently change or become obsolete, this list may be of dubious value.
The huge retrospective epidemiological study of GDV, as I mentioned above, is at Purdue, run by Larry Glickman. The project was funded by the AKC Health Foundation and by breed clubs.
Very close to where the stomach empties its contents into the small intestine, ducts contribute secretions from the gall bladder and pancreas, mostly to aid in the metabolism of fats, which are fairly resistant to action by gastric acid. If either gland does not function properly, this can result in loose stools and inefficient absorption of nutrients, with highly variable severity.
The pancreas is a rather long, V-shaped gland located near the stomach, and aids the digestion of food. It has two major types of cells or tissues. One group is endocrine in nature, which means it secretes hormones into the circulatory system, which in turn transports them to other glands and body parts. The endocrine activity of this gland serves to control blood sugar level, and when defective, results in diabetes. The other, exocrine, part empties a group of biochemicals into the digestive tract. It produces enzymes and bicarbonate, and excretes these into the duodenum, which is the first short section of the small intestine. One major enzyme, amylase, breaks down the long starch macromolecules, while others break down fats and proteins. Most GSD people, in America, at least, are concerned more with the digestive function than with diabetes. I have corresponded with fanciers in England who are concerned about pancreatic insufficiency, and since many of their lines are from recent German imports, this is possibly a more widespread problem there than I had earlier suspected. I know I have seen the occurrence in pancreatic insufficiency increase among the German lines in the U.S., but that might be because more and more people are turning away from the American GSD for many other reasons.
Exocrine pancreatic insufficiency (EPI) is a condition in which that part of the pancreas stops producing and secreting enough digestive enzymes and bicarbonate to properly digest food in the small intestine. Severity may vary between individuals, and even vary in one dog from time to time. Diarrhea and foul-smelling feces due to high undigested fat mark the condition known as steatorrhea, and because food ingredients are not being digested the animal becomes malnourished; in many cases nutritional deficiency as well as energy deficiency results. The cause of EPI can sometimes be traced to another primary pancreatic disease, or from any disease that interferes with enzyme secretion or action in the intestine. Juvenile pancreatic atrophy and chronic pancreatitis are the most common, but other causes include obstruction of the pancreatic duct (by a tumor, for example) which ordinarily carries the enzymes into the lumen of the duodenum.
Clinical pancreatitis — The word clinical may be used to mean “frank” or “obvious”, at least to a veterinarian with the training and equipment. Any disorder with “-itis” on the end refers to an inflammation. Most causes of this disorder are of unproven origin, but “bad genes” must be the prime suspect. Adult clinical pancreatitis is not tremendously common in the German Shepherd Dog, but when it does occur it is usually the middle aged, obese bitch on a fatty diet that has it. Symptoms of chronic pancreatitis (recurrent inflammation of the pancreas) include emaciation, dull dry coat, and high appetite with poor digestion as seen by fatty, loose stools containing undigested starches. Treatment is aimed mainly at correcting the diet, but it is very difficult to control.
Pancreatic atrophy — On the other hand, German Shepherd Dogs seem to have a considerable predisposition to pancreatic atrophy, also known as juvenile atrophy or pancreatic insufficiency (PI), and certain bloodlines have been much more associated with it than others. For years I have referred to the milder manifestations as subclinical pancreatitis, because people who are not familiar with familial and breed tendencies are likely to miss the subtle signs, and I had suspected the two forms were variations of one basic problem. EPI can be subclinical for many months or even years before it worsens or is classified as chronic and acute. The disease usually starts before the dog is one year old, though many are three before symptoms are noticed. When lack of “drive”, diminished coat lustre, coprophagia, and/or poor weight are seen, have the stool examined by your veterinarian for abnormal fat level and absence or low level of the trypsin enzyme.
If the problem is discovered before it becomes severe and chronic, Viokase™, a brand of powdered raw pancreas, added to the food half an hour or more before feeding usually produces good results. Other similar products that I am familiar with are Pancreazyme™ and Prozyme™. I have heard of a British product called Tryplase as well. I was told, but have not verified this, that Prozyme “is not the medication of choice as it only contains the vegetable type enzymes.” Costs vary widely among these. Getting enough to do the job without making the owner go broke is a tough balancing act, though. By the way, these types of preparations also appear to be good for non specific diarrhea. I believe there is a strong possibility that subclinical pancreatitis can worsen with neglect into an acute attack by enzymes on the pancreatic and surrounding tissues themselves, and that this condition may be the cause of many instances of diagnosed perforated ulcers. Texas A&M vet school at one time was trying to get AKC and GSDCA funding to study and possibly identify a genetic marker for pancreatic acinar atrophy in the breed. The cause of pancreatic acinar atrophy has been determined to be an immune system deficiency.
Malabsorption or poor digestion and stool condition (soft, mushy) are frequently seen in the GSD, and in my experience, has been more so in the heavily linebred typical lines in American-bred dogs since the 1970s. EPI (whether frank or sib-clinical) is one of the conditions that can contribute to the malabsorption syndrome. The symptoms can be exacerbated by physical or emotional stress, change of food, and other things. I suspect that dogs with subclinical weakness in immune systems or pancreatic function may be most likely to show these reactions. I know that my strongest-character dogs over the years have also been able to eat almost anything without diarrhea. Others have also proffered the theory of an abnormality in the immune system. Such dogs are apparently more likely to show symptoms like increased susceptibility to bacteria, intolerance to change in diets, ravenous appetite, reduction in body weight or failure to gain, diarrhea, greasy-looking feces with possibly undigested cellulose as well, and an “unthrifty” dry coat. The usual response by breeders and vets is to try the enzyme supplements and/or something like Hills Prescription Diet. But there are about as many stories of failure as there are of successful (though tricky, difficult) control. Some believe that an increase in roughage or “bulk” is needed in order to “keep the food in the system” long enough for the digestive system to do its work, but others say that more bulk or roughage tends to make it harder to control. Also, we are told to feed our affected dogs low-fat foods but not deprive them of the essential fatty acids. Indeed, it is a frustrating battle that many owners engage in.
The Animal Health section of HelpLine (a UK website), autumn 1999 issue had several articles on frank pancreas insufficiency and malabsorption. It reported that the trypsin method (Tli) replaced the fecal test, which had proved inaccurate. Differential diagnosis of pancreatic insufficiency and other small intestine disease are sometimes difficult since clinical signs can be similar. Many problems that befall the GSD point to autoimmune conditions; research was carried out by Dr. D. Williams in the U.K. in this regard. Pedigrees have been requested by veterinarians working on this problem, and a clearinghouse for information has been set up by Dorothy Cullum, 15 North Road, Brentwood, Essex, England. For further reading on the subject, contact her:
Some owners with access to slaughterhouses claim some benefit from feeding raw pancreas, but there is not enough data with scientific controls to consider this anything more than anecdotal testimony. This is not to discount testimonials, though, as these can lead to success and may be incentive for scientific corroboration. One reader in the UK tried the natural pig pancreas plus roughage route, and said that the pancreas from the abattoir “is no more unpleasant to handle than any other meat from the freezer, costs half the price of powdered enzymes, the dog absolutely loves it and appears to be more effective than any man-made preparation on the market! He is not requiring as much food, as he is obviously absorbing what he needs from his diet now. He is not full of wind, and he is now producing approx. 1/3 of the amount of faeces that he did on the powders. I have also noticed that he is no longer ravenously hungry and has actually left some of his dinner on a few occasions.” On the other hand, many experts say that you should reduce the amount of non-digestible fiber in the diet for dogs with pancreas problems.
Treatment is nutritional—it involves the use of replacement pancreatic enzymes given orally, if you are not so fortunate as to have access to an abbatoir. If you choose the expensive specialized EPI diet foods from Hills, Eukanuba, or others, check the labels and prices—they are “out of sight”. People who treat their EPI dogs for the rest of the dogs’ lives can spend about $1,000 to $1,500 annually for the enzymes alone. If you go along this road, you will have to “soak” the ration for a while, to give the enzymes time to work—longer for the dry rations than for the canned. The enzymes have their greatest effect after a soak of about 20 minutes.
Suitable products are available in powder or crushed non-enteric coated tablets. Enteric-coated tablets are not usually recommended because dissolution of the coating by alkaline pH in the intestine is unreliable. Because some enzyme is denatured by acid in the stomach, premixing the enzyme supplement with the food and left for about three quarters of an hour at room temperature is usually recommended.
According to at least one commercial enzyme powder producer, ProVet, medications such as receptor inhibitors (e.g. Cimetidine) can also be useful because they reduce gastric acid secretion; thus, less pancreatic enzyme is denatured during passage through the stomach. If bacterial overgrowth is present, oral antibiotics may be indicated as well. With enzyme replacement and cimetidine and/or neomycin, fecal fat concentrations can be returned to normal.
The following dietary management is recommended by ProVet (email@example.com):
- Feed a highly digestible, palatable, complete ration. Avoid home made rations.
- The ideal profile is a diet that is low in fat content, but contains medium-hain fatty acids.
- Avoid foods with excess carbohydrate and low fiber.
- Feed multiple small meals (at least 3 times daily).
A dog owner wrote to me and said, “I want to try your recommendation of fresh pancreas fed to the puppy with chronic diarrhea. How much do I give and how often? At every meal? And, I assume it is given raw.”
Given the variety of symptoms and needs of different dogs, it’s impossible to accurately measure how much enzyme the dog will need, or how much benefit it may do him. Best bet is to treat raw or cooked pancreas as any meat supplement: no more than 25% of the daily ration. Probably 10% is a good starting point for experimentation. Just estimate. If you get better results with larger percentage, go for it. Remember that there are many factors, and the dog’s needs may change daily. Keep other fats in the diet very low… get a low-fat but highly digestible commercial dry food as your base. I would try 10% replacement with cow or pig pancreas and another 10% with lean meat like chicken. One problem with living in Alabama is that there are regulations against selling stuff such as past-date cottage cheese, cracked eggs, organ meats, etc. Residents of our fair state have to have a friend “on the inside” at some slaughterhouse or wholesale butcher or manager of a store meat dep’t. Yes, raw is probably better, as cooking can destroy some enzymes. I think the Viokase people freeze-dry their product so they can sell it as a ground powder. Yes, I would feed it at every meal, so I would have it chopped, cubed, or ground, and make patties to freeze, thawing out a couple every day.
Warning: you can spin your wheels for years on the abundance and infinite variety of nutritional advice. Many claims are entirely unrelated and coincidental to results, but people who are desperate will tend to try them all. Another correspondent told me that, after initial help, she was no longer getting satisfaction by using just the enzymes; her dog’s stools were getting poor again. Later, she found good maintenance results by supplementing with folate, vitamin B-12, banana, live-culture yogurt, oatmeal, baked yams, and flaxseed oil (for those fatty acids) twice a day, in addition to “one cimetidine tablet (brand name is Tagamet) morning and evening, three times a week”. Cephaloxin 500 mg two or three times daily, depending on the situation, is sometimes administered for two weeks. This diet change had followed the Texas A&M College of Vet Medicine’s suggested treatment with cobalamine folate. Cobalamine is vitamin B-12, and folic acid (obtained synthetically or in liver, green leaves, and yeast) is essential to the friendly lactobacillus in the gut, in combination with which it inhibits malabsorption. That lady did not see a turn-around in condition until more B-12 was added to the vet school’s recommended treatment. She found that 2,000 milligrams of folate and a fourth-teaspoonful of liquid B-12 with the dog’s light meals three times a day gave marked improvement It appears that occasional (quarterly, for example) antibiotic treatment to kill unfriendly bacteria, followed by folate and yogurt to encourage the lactobacillus, is highly thought of by veterinary nutritional specialists. I am a fan of vitamin E, having seen benefits in many areas, so I always recommend that people also give one or two 400-IU capsules a day of Vitamin E to help boost the immune system.
Most people make a distinction between EPI (Exocrine Pancreatic Insufficiency) and pancreatitis, some saying that dogs can recover from pancreatitis, the rather simple inflammation of the pancreas, and that when the pancreas begins to atrophy, the only thing you can do is supplement with digestive enzymes like Viokase V or with Pancreazyme. I tend to believe the two conditions are more intrinsically linked. Canned dog foods, even the non-prescription brands, are said to be easier for the EPI dogs to digest than is dry kibble, although they tend to produce more flatulence. The EPI dog is unable to efficiently digest carbohydrates, protein and especially fat. The condition is also called acinar atrophy, the word “acinar” referring to the physical tissue structures that make up lobules in the gland. When the pancreas atrophies, it loses ability to function in its digestive mode; it apparently does not interfere with insulin production, which is its endocrine function carried on by different types of cells. Some dogs do become diabetic as well, but this may be entirely unrelated.
I have been told that the statistics on EPI dogs indicated that 1 in 5 pups born to an EPI-affected dam would eventually show signs of EPI. There seem to be a higher than average number of stillborn pups, as well. Whether this has anything directly (genetically) to do with EPI, or is a reflection on the poorer physical condition that leads to uterine inertia, is hard to say. By the way, on the website you are now surfing or may soon, you might also find my article on uterine inertia and the use of oxytocin.
Increased gut sounds are often noticed by the owner or the vet. Sometimes we see a pallor in the gums due to anemia and low concentrations of circulating blood protein. But EPI diagnosis needs to be confirmed with lab tests. The most-used test for dogs is the Trypsin like immunoreactivity (Tli or TLI) test, but other tests are often employed, and may still be needed in complicated cases that have more than one concurrent disease. Microscopic views of stool samples and lab tests for fecal fat are often used. The Tli test that your vet or his contracted lab will perform determines the levels of digestive enzymes like trypsin that are present. It can vary from day to day, even increasing and decreasing and varying within the same day. The scale on this test from low to high, is 5.0 to 35.0 while GSD’s rarely test over the 5.0 to 8.0 range. At Texas A&M, the researcher tells us they have found that dogs that normally test below 8.0 will most probably become EPI positive.
Description: The TLI test is highly sensitive and specific for the diagnosis of canine exocrine pancreatic insufficiency (EPI). This test measures the concentration of trypsin like proteins in a blood sample by radioimmunoassay. These proteins diffuse into the blood stream in small amounts (0.01 to 0.1% of pancreatic trypsinogen).
- In normal dogs the TLI concentrations are greater than 2.5pg/L (up to 35pg/L).
- In dogs with exocrine pancreatic insufficiency, TLI concentrations are less than 2.5 pg/L
- In dogs with pancreatitis, TLI can be normal or increased.
- Dogs with bacterial overgrowth have a normal TLI test unless exocrine pancreatic insufficiency is present as well.
- False negative results may occur if a dog has concurrent pancreatitis (increasing TLI) and exocrine insufficiency
Above paragraph and list copyright 2003, Provet. Email: firstname.lastname@example.org uk
Of course they are talking about all breeds, and we must remember that there are breed differences. The GSD, for example, has a higher packed-cell volume than other breeds, and it is likely the Tli range that is abnormal for others might be more normal or manageable for GSDs. The disorder might remain fairly unnoticed or asymptomatic until it reaches a Tli much below 5.0, then the dog typically begins to get voraciously hungry and has terrible diarrhea with a sour odor, many times a day. Severe weight loss is an indication that the dog is starving to death. The fur loses pigment and gloss, becomes dry and brittle and often is lost to some extent, and Staphylococcus infection scabs may appear on the skin, because the compromised immune system doesn’t allow the dog to fight off the infection. The symptoms of EPI mostly show up when the TLi is down around 2.5 to 3.0. In most breeds perhaps, any dog that tests at even an 8.0 will be at high risk for EPI. So, most dogs will be diagnosed with EPI when Tli is at 8.0 or less, and perhaps 0.4 or lower for GSDs. If a dog is found to be within the normal Tli range (for GSD’s 5.0 to 8.0) but exhibits symptoms such as much flatulence, diarrhea that is light brown/yellow to clay color from time to time, the dog should be tested for levels of Lipase, Protease and Amylase.
I had corresponded with a lady in Michigan named Dee, who had much personal experience with EPI. She and others discovered that even if the test shows the dog to be in the 8 range on the scale, it’s quite likely that the dog has developed EPI, or will in the future. Other breeds seem to test higher, such as 15 to 35. GSDs are noted for having notoriously low TLi’s. The condition is widespread in the breed, probably due to considerably tight inbreeding on “carriers”. The higher the reading is in a GSD, the better; it indicates that the dog is digesting normally. Not all GSDs are symptomatic, but any unexplained diarrhea and weight loss, a voracious appetite, frequent stools that are runny or like pudding in firmness, or are pale colored, such as putty gray, or dark mustard yellow, and of a sour foul smelling type, are good reasons to have the dog Tli-tested, to determine if the pancreas is failing. With this condition the dog is not necessarily diabetic, as the condition does not affect the endocrine portion of the pancreas. However, if the dog has also developed diabetes, then it is extremely difficult to treat the dog, and one would wisely consider putting his dog out of such a miserable state.
Dee says: “If one breeds one dog that is a carrier of the EPI gene(s) to another who is also a carrier, it is most likely all the pups will be affected. Statistics of a few years ago indicated that one in every five pups will be affected if only one parent is “diagnostic” for EPI. Another article said that one in four would be affected. This condition can show up any time from birth on, if the pups come from parents who both carry the gene for EPI. If only one parent is a carrier, then the odds of escaping symptoms are improved. For this reason some recommend that only males be given the TLi to see what range they are in, prior to breeding. If both dam and sire are “testing low”, we would advise not breeding them. Only the GSDs with the highest readings and without any “marker gene” should be bred. Dee feels that the breeding pair should be tested at least twice before being bred instead of finding the problem later, after one realizes that they’ve produced litters of defective dogs that will die a terrible death if not treated.
We must also consider the owner on limited income who cannot afford to treat a dog for its lifetime, a dog that perhaps should be destroyed. Even if the person can afford to treat the dog for its lifetime, but the enzymes stop working, or are just plain ineffective, the dog will probably still have to be euthanized. The TLi varies from time to time, so one will not necessarily get the same reading twice, but if the dogs regularly test low, castration or spay would certainly halt the genetic progression. Being recessive, EPI is the kind of condition that one cannot easily “breed out”. It’s up to the good breeders to control this condition.
In general, many dogs who test at 8.0 have been known to develop EPI as they get older. Apparently they are carriers, and may not necessarily show symptoms early in life. Occasional bouts with diarrhea may be insufficiently diagnosed as idiopathic “gastroenteritis” at the time, and get treatment that only temporarily seems to resolve the problem. Dogs with a history of bloating/torsion and/or bouts of unexplained diarrhea are reportedly quite likely to be EPI-carrier suspects, although this observation is purely anecdotal. EPI occurs most frequently in dogs, and rarely in cats. The German Shepherd Dog is the breed most likely to be presented with EPI and/or pancreatic atrophy. The popularity and high population of the GSD breed may be a factor in this seeming phenomenon, and close inbreeding practices may have some influence. It certainly seems that the American lines are plagued far more than the German lines are. Some people perceive a probable connection or coincidence between anal furunculosis (perianal fistulas) and EPI. A great deal of the digestive system may be affected one way or another. In Finland, the Rough coated Collie is also predisposed to develop EPI.
The genetics of pancreatic disorders may confuse, because the expressions are highly variable. Some can carry the trait and never develop EPI, while others show symptoms, although the genotype may be similar. The wisest recommendation is that such dogs not be bred as they most certainly carry the recessive gene. They are currently looking for a “marker” in the families of dogs they’ve been working with over the last couple of years. Before breeding, one perhaps should have the TLi test done, and get a hint of the possibility of carrying the gene. If you breed two that are carriers together, you risk as much as the entire litter having EPI. I once bought a full brother of a famous champion named Paladen; my “Harry” was a beautiful animal with excellent hips, but he developed the pancreatic disorder and had to be controlled as much as possible with the Viokase enzyme powder. I had sold a co-ownership in him before the disorder developed, and he was killed in a car crash before many years of treatment and follow-up would have been completed. Some other fanciers with close relatives also reported pancreatic insufficiency in their dogs. Many dogs can have an extended lifespan, but some die soon after the disorder strikes.
One vet I know of told his client that EPI “is not considered being ill—merely a genetic condition.” Merely a matter of semantics? To me, pancreatic insufficiency is an abnormality that calls for removal from the gene pool, whether the dog has a severe or a mild case or is asymptomatic most of the time. I have found that most vets take but a modicum of hours of nutrition and practical genetics classes in vet school, and then forget most because they don’t use it every day. Breeders, especially those with a science background, are more reliable sources of information, I think. Unfortunately, not many people who offer their EPI males at stud admit or declare any cautions about their dogs. As one observer quipped, “It’s funny isn’t it, that those who deny all those things have Viokase-V on the shelf in their back rooms?” Yes, in spite of the fact that it is good for various unspecified causes of diarrhea, it is so much more expensive than Kaopectate that it makes you wonder.
Connection between PI (pancreatic insufficiency)and GDV (bloat-torsion)? There have been reports from dog owners indicating that many episodes of EPI begin either with a bloating incident, or with a gastroenteritis, marked by vomiting and blood tinged diarrhea. One who had “chatted” on the Internet with many GSD owners in the UK and the USA said, “From the general info collected, the dog first bloats, which often leads to torsion of the gut, which of course requires surgery for a tacking of the stomach, and this is usually followed by a full blown episode of EPI within a few months of the surgery.” I have not seen much evidence of such a connection, but data is sparse.