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Pancreatic insufficiency in dogs: symptoms and treatment of TSD in dogs

Pancreatic insufficiency in dogs

Pancreas - inconspicuous organ lying in front of the abdominal cavity.

An organ that is talked about a lot, but doesn't really know much.

It performs its functions quietly and imperceptibly, but hardly anyone appreciates her work.

Every dog ​​or cat keeper is aware of the importance of such organs as the heart, liver and kidneys.

But the pancreas? Who cares about her?

Well, maybe caregivers of diabetic animals recognize its role in insulin production.

However, these are only part of the tasks facing this important, but often overlooked in diagnostics, organ.

Let me outline in this article what an essential and unsurpassed organ the pancreas is, how many functions necessary for life, what happens when this perfect chemical factory begins to refuse to obey, and how to deal with the consequences pancreatic insufficiency.

  • What is the pancreas?
  • How the dog's pancreas works?
  • When the pancreas gets sick
  • What is pancreatic exocrine insufficiency?
  • Causes of pancreatic insufficiency in a dog
  • Which dogs are most at risk of developing ATS?
  • Pathophysiology
  • Pancreatic insufficiency in dogs symptoms
    • Laboratory tests
  • Diagnosis of TSD in a dog
    • CTLI test
    • Fecal pancreatic elastase 1 activity
    • Other research
  • Differential diagnosis
  • A subclinical form of pancreatic insufficiency in a dog
  • Secondary and accompanying ZNT diseases
    • An overgrowth of bacterial flora in the small intestine
    • Cobalamin deficiency
    • Torsion of the mesentery
  • Treatment of dog pancreatic insufficiency
    • Pancreatic insufficiency in dogs
  • Treatment of subclinical NNT
    • Side effects of enzyme administration
  • Pancreatic insufficiency in the dog's diet
    • Support diet
  • Monitoring a sick dog
  • Side effects of therapy
  • Dog pancreatic insufficiency and prognosis
  • Prevention

What is the pancreas?

Structure of the dog's pancreas | source: wikipedia

Pancreas it is an elongated, loop-shaped organ in a dog sandwiched between three essential neighbors:

  • the liver,
  • stomach,
  • duodenum.

In terms of development "partner " liver, is a classic example of a mixed gland that functions both exocrine, what endocrine, that is endocrine.

The exocrine pancreas, which is the main mass of the organ, is the follicular gland.

From a functional point of view, it is panlitic gland, which means that the pancreatic juice produced by it contains digestive enzymes that "attack " all food components:

  • carbohydrates,
  • proteins,
  • fats.

This follicular part definitely dominates the endocrine (endocrine) part, represented by very small (microscopic) structures - the so-called. pancreatic islands (formerly known as the islands of Langerhans), suspended in the flesh of the organ like "raisins in dough ".

It is the cells grouped in the islands that fulfill the endocrine production role insulin, glucagon and somatostatin - hormones controlling the metabolism of mainly carbohydrates, but also fats and proteins.

It is impossible to estimate which of the components of the pancreas is more important, both have completely different functions, both cannot be overestimated.

Both endocrine and exocrine dysfunction are conditions that require a firm therapeutic approach and when they occur, it indicates damage to a part of the organ and the need for treatment.

How the dog's pancreas works?

The endocrine part of the pancreas produces hormones, regulating blood glucose metabolism.

Endocrine mechanisms and a disease associated with disruption of endocrine function are described in the article on diabetes in dogs and cats.

In this study, we will deal exclusively with digestive function of the pancreas.

The exocrine part of the organ produces, as already mentioned, a series of digestive enzymes to digest carbohydrates, fats and proteins.

Protein digestion is catalyzed by trypsin, chymotrypsin and carboxypeptidase.

These enzymes are initially released from the pancreas in the form of so-called. zymogens (i.e. inactive starting forms of enzymes - the pancreas thus protects itself against self-digestion).

These are respectively:

  • trypsinogen,
  • chymotrypsinogen,
  • procarboxypeptidase.

After reaching the intestine, they are activated.

Under the influence of the presence of food content in the lumen of the small intestine enterocytes (i.e. the cells of the intestine) release enteropeptidase, which activates trypsinogen.

At this point, trypsin is formed, the second task of which (apart from the breakdown of proteins) is to support the activation of all three zymogens.

When activated, trypsin and chymotrypsin break down proteins into smaller peptides and carboxypeptidase ends the matter by breaking down shorter peptide chains into amino acids.

Digestion of carbohydrates is possible thanks to pancreatic amylase, which hydrolyzes most carbohydrates to disaccharides and some trisaccharides.

The digestion of fats is assisted by release by the pancreas pancreatic lipase, cholesterol esterase and phospholipases, and zymogen procolipase (activated by trypsin to colipase).

Pancreatic juice is not only digestive enzymes, but also calcium bicarbonate in the form of an aqueous solution.

The release of digestive enzymes occurs upon stimulation by acetylcholine and cholecystokinin, while bicarbonate and water are released under the influence secrets.

Sodium bicarbonate, found in the lumen of the duodenum neutralizes gastric secretions.

The weight of a dog's pancreas varies from about 15 to 108 g (depending on the size of the dog).

Now imagine that this organ, weighing about as much as a plum (in gusts up to a medium-sized banana):

  • produces up to 2 liters of pancreatic juice daily (which includes all the above-mentioned enzymes),
  • regulates the metabolism of fats, carbohydrates and proteins,
  • keeps blood sugar levels in check,
  • provides adequate microflora in the intestines,
  • enables the proper absorption of vitamins (mainly cobalamins).

A lot of this for such a "meager" organ.

The worst thing is that if something bad starts happening within it, you don't see symptoms for a long time

The pancreas is sick in silence at first.

Despite its vulnerability to damage, it has a disastrous trait huge functional reserve.

This means that only when damage occurs over 90% of the organ, clinical signs begin to become apparent.

When the pancreas gets sick

A sick pancreas in a dog

Taking into account the functions of the pancreas, it can undoubtedly be compared to a small, albeit very efficient and precise chemical factory, whose task is not only to absorb and break down food ingredients, but also to ensure that the products of their decomposition (especially sugar) are at all times in the optimal amount in the blood.

Quite a lot of tasks for such a small and insanely sensitive gland.

But the pancreas, as a rule, does its job very well.

It happens, however, that - for various reasons - something begins to fail in the mechanism and disturbances appear.

If they affect the endocrine part of the organ, clinical symptoms develop diabetes.

If, in turn, the damage applies to acinar cells of the pancreas - the condition known as exocrine pancreatic insufficiency.

Then it comes to digestive disorders and absorption of nutrients.

The presence of undigested food in the lumen of the gastrointestinal tract promotes the overgrowth of abnormal bacterial flora, which additionally impairs bowel function.

Occur loose stools, diarrhea in a dog. The animal has a huge appetite, but is losing weight.

Often times, owners find it looks as if the food has literally "flew" through the dog.

Fortunately (or unfortunately) the pancreas has a large functional reserve, which is why such symptoms are visible late - when a significant part of the organ has already been damaged.

What is pancreatic exocrine insufficiency?

Pancreatic exocrine insufficiency/ZNT (exocrine pancreatic insufficiency / epi) is a deficiency in digestive enzymes.

It is a disease syndrome consisting of the abnormal synthesis and secretion of pancreatic digestive enzymes as a result of severe damage or lack of acinar cells in the pancreas that produce enzymes.

Probably the most typical symptom and - at the same time - the first motive for consultation in a veterinary office - is chronic diarrhea from the small intestines or loose stools.

Causes of pancreatic insufficiency in a dog

The most common development of SCT in dogs is due to the disappearance of acinar cells in the pancreas.

In 50% of cases, EPI is caused by pancreatic acinar atrophy (PAA).

Idiopathic PAA is the most common cause of EPI in German Shepherds and long-haired scottish shepherd dogs.

Acinar cell atrophy is considered to be an immune-mediated phenomenon that begins with lymphocytic pancreatitis.

As the process continues, the acinar cells of the pancreas are selectively destroyed, which in turn are replaced by abnormal parenchymal cells, tubular structures and adipose tissue.

In this way, the pancreas slowly turns off its exocrine functions.

Ultimately, tissue destruction, necrosis and apoptosis of secretory cells occur.

Chronic pancreatitis is the second - after PAA - cause of destruction of acinar cells in this organ (all breeds of dogs are at risk, but Cavalier Kings Charles Spaniels and Jack Russell Terriers are strongly predisposed).

Subsequent pancreatic fibrosis after pancreatic inflammation may involve islet cells in the endocrine part (this leads to the development of diabetes) and / or acinar cells in the exocrine part (then SCT develops).

Other rare causes may be:

  1. Pancreatic duct obstruction (e.g. due to tumors or surgery). It happens (fortunately rare) that the tumor obstructs the pancreatic duct, preventing the release of digestive enzymes into the duodenum. Although the capacity of the pancreas to produce digestive enzymes may be unchanged, they fail to reach their target site and clinical signs of TSD develop.
  2. Congenital aplasia or pancreatic hypoplasia. It has been suggested that congenital underdevelopment of the pancreas causes the disease mainly in puppies.

Risk factors:

  • racial predisposition,
  • factors predisposing to chronic pancreatitis.

Which dogs are most at risk of developing ATS?

Which dogs are most at risk of suffering from znt?

Exocrine pancreatic insufficiency can occur in all breeds, but is especially common in German Shepherds.

Approximately 42% of all affected dogs are of this breed, the other being the longhair Scottish Sheepdog.

It is believed that in representatives of both of these breeds, the disease is conditioned genetically (autosomal recessive gene).

ZNT quite often also occurs in Cavalier King Charles Spaniels (often caused by chronic pancreatitis), Chow Chow dogs and Irish Setters (usually the disease develops as a result of progressive atrophy of acinar cells or underdevelopment of the pancreas).

It is also found in cocker spaniels and West Highland white terriers.

In females of the above-mentioned breeds, the disease is slightly more frequent, but the sex does not have a major predisposing role.

The average age of dogs that develop symptoms of SST is variable, strongly correlated with the cause of the disease.

Dogs with EPI in the course of PAA are usually young, adult dogs, aged about 1-2 years.

Patients with exocrine pancreatic insufficiency as a result of chronic pancreatitis are common middle-aged, nevertheless, the disease can affect dogs of all ages.


The loss of acinar cells leads to a lack of digestive enzymes in the small intestine, resulting in nutrient absorption and transport disorders, which is manifested by loose, voluminous stools and weight loss.

Undigested food debris can modify the intestinal microflora, and as a result it appears dysbiosis.

The gastrointestinal mucosal trophic factors, peptide regulators and intrinsic factor are also insufficient, leading to changes in the functions and structure of the mucosa of the small intestines.

Generalized malnutrition affects the gastrointestinal mucosa.

Sometimes in patients with EPI diabetes develops secondary to chronic pancreatitis, but this is unlikely to occur in patients with PAA.

Pancreatic insufficiency in dogs symptoms

Pancreatic insufficiency in dogs symptoms

The clinical symptoms that develop in this syndrome are generally attributed to poor digestion and absorption of nutrients.

Symptoms of pancreatic insufficiency in a dog appear when it disappears or is damaged approx. 90% of the glandular cells, and the secretion of enzymes will drop below 15%.

Exocrine pancreatic insufficiency is manifested primarily by symptoms from the side digestive system:

  1. The most prominent symptom is weight loss despite normal or increased appetite. Dogs eat whatever is offered to them and still appear hungry. Occasionally, however, there are episodes of weakness or even loss of appetite.
  2. They most often accompany the progressive weight loss foul, loose stools. It may appear initially in dogs severe watery diarrhea. Often noticeable too:
    • the presence of fat in the stool,
    • flatulence in a dog,
    • a rumbling in the belly.
  3. Feces, as a rule yellow or lead gray color, tends to be mushy, pasty and / or contains undigested food residues.
  4. The volume of the feces is definitely increaseda, and the consistency can be compared (inelegantly) to "cow pie ".
  5. The number of defecations during the day is increased (usually> 3 in one day).
  6. Eating disorders are possible, such as coprophagia or even eating inedible items.
  7. Some dogs with TSD vomit, but this is a rare symptom.

If it shows up increased thirst and urination (characteristic of severe cases), it is associated with the development of endocrine pancreatic insufficiency and diabetes.

Animals can make an impression irritable, nervous or even aggressive - this is due to abdominal discomfort (rare symptom).

Insufficient digestion and absorption of nutrients leads to death in untreated dogs due to deficiency and exhaustion (even despite eating large amounts of food).

In the clinical trial, the following are in the foreground:

  • poor body condition and muscle atrophy,
  • severe emaciation,
  • poor quality of the coat, resulting from mineral and vitamin deficiencies.

Laboratory tests

Exocrine pancreatic insufficiency rarely causes changes in blood counts or serum biochemistry.

Certain disorders can occur, but they are non-specific and have no diagnostic value:

  1. Blood count - usually insignificant.
  2. The activity of serum amylase and lipase is irrelevant in the diagnosis of NTS.
  3. Occasionally, serum tests show hypercholesterolaemia, caused by disturbances in fat digestion.
  4. Increase in the level of alanine transaminase, aspartate aminotransferase and alkaline phosphatase - the reasons for the elevation of liver parameters in the blood in the course of TS have not yet been clarified. One theory is that it results from the increased absorption of hepatotoxins by the impaired wall of the small intestine and their destructive effect on the liver.
  5. Hyperglycaemia in patients with coexisting diabetes.
  6. Serum folate levels may increase.
  7. The concentration of cobalamin is decreased in over 80% of patients.

Diagnosis of TSD in a dog

Diagnostics when epi is suspected

History and clinical symptoms may lead to suspicion of EPI, but symptoms are not specific enough to distinguish between TSF and other digestive disorders.

CTLI test

Testing of trypsin-like immunoreactivity - the final diagnosis is made precisely on the basis of cTLI.

This species-specific test is used for the qualitative determination of serum trypsinogen and trypsin.

cTLI is an immunological test that measures the concentration of trypsinogen that has entered the blood directly from the pancreas.

The physiological values ​​of cTLI in dogs vary widely 5-35 μg / L.

  • When the concentration of cTLI < 2.5 μg / L after withholding food for> 8 hours - the result confirms exocrine pancreatic insufficiency.
  • Concentration in between 2.5 and 7 μg / L may be associated with a latent EPI. In this case, the test should be repeated after 1-2 months.

The decreased concentration of cTLI is highly sensitive and specific to EPI and is not dependent on enzyme supplementation.

So what can affect the test results?

The test results may change when you have pancreatitis, although they are not affected by any eventual pancreatitis an inflammatory process in the gut. If the inflammation affects debris of the organ's active acinar cells, the cTLI result may be falsely elevated.

Another situation in which the result may be distorted is the same as ZNT kidney disease.

Since trypsinogen excretion is via the kidneys, dogs with kidney failure may even achieve normal cTLI values.

CTLI levels may be normal in patients with exocrine pancreatic insufficiency developing secondary to pancreatic duct obstruction.

A false elevation of cTLI may also be the result of postprandial sampling.

It is safest to take a blood sample for testing from a patient who has stayed starved for at least 12-18 hours.

Haemolysis also affects the test results.

Despite these few factors that may interfere with the correct interpretation of the results, this test is 100% sensitive and specific in the detection of exocrine pancreatic insufficiency, if you get the result < 1,9 μg/L.

Fecal pancreatic elastase 1 activity

This enzyme-linked immunosorbent assay does high sensitivity but low specificity.

Type 1 pancreatic elastase is a zymogen that is produced exclusively in acinar cells in the pancreas.

The enzyme also passes through the intestines unchanged, and is not affected by intestinal inflammation.

Due to the fact that this is a species-specific test, the administration of pancreatic enzymes does not affect the result.

  • Concentration < 10 μg / g feces - confirmation of ZNT (it is worth to confirm it with the cTLI test).
  • Values> 40 μg / g feces - pancreatic exocrine function is normal = ZNT excluded.

Values ​​in the interval 10 - 40 μg / g feces considered borderline.

Additional tests should then be carried out.

Other research

In the past, before the introduction of the radioimmunological cTLI method, other tests were used to determine the function of the exocrine pancreas. They included:

  1. Fecal Proteolytic Activity Test (which should be low in dogs with TSD):
    • The simplest and most traditional method was microscopic examination of feces. Fresh faeces samples had to be mixed with dye (Sudan III) and 2% Lugol's solution. Sudan III showed orange-colored fat drops, and Lugol's liquid showed dark blue-colored starch grains.
    • Radiographic film test (the so-called. film test). The faeces is mixed with a 5% solution of sodium bicarbonate, a strip of previously developed X-ray film is placed in such a suspension and its color changes are observed. If the proteolytic activity of the fecal enzymes is adequate, the blackened X-ray film will turn bright. However, in the case of ZNT and low enzymatic activity, the film will not discolor. Since faecal proteolytic activity may be reduced in some animals with normal pancreatic function, faecal tests may be indicative character.
    • The method of azocasein.
    • Method radial diffusion of enzymes.
  2. Activity tag chymotrypsins in feces. A drop of fecal suspension is applied to the plate containing the chymotrypsin-degraded substrate. The higher the enzyme activity, the larger the zone of brightening around the stool sample.
  3. Test with n-benzyl-L-tyrosine-p-aminobenozoic acid in serum (NBT-PABA) - as an indirect method of detecting chymotrypsin in the blood. It is based on the oral administration of N-benzyl-L-tyrosyl derivative of para-aminobenzoic acid. As a result of passing through the digestive system, this compound is selectively broken down into para-aminobenzoic acid (PABA). The resulting PABA is then absorbed into the body. Ultimately, its level in the blood serum is determined. In healthy patients whose pancreas is functioning properly, the amount of PABA in the test sample should be high. This means that the pancreas is secreting enzymes properly. In the case of its exocrine insufficiency, pancreatic chymotrypsin is insufficiently secreted and the conversion of NBT-PABA into para-aminobenzoic acid does not take place.
  4. Starch tolerance test.
  5. D-xylose absorption test. A change in the consistency of the faeces to be liquid or mushy, their foul smell and the presence of undigested food debris in the faeces are not specific symptoms of exocrine pancreatic insufficiency, especially in dogs. Similar symptoms may accompany other diseases, mainly of the intestines (although it is especially pronounced in the case of TSD). In order to distinguish between these states were performed xylose test, which consisted in the oral administration of D-xylose at a dose of 0.5 g / kg m.c., and then its plasma concentration was determined at 0, 60, 120 and 180 minutes after administration. In healthy animals and animals with AN, there should be a large increase in the concentration of D-xylose (up to over 45 mg / dL), usually highest at the 60th minute. In animals with gut dysfunction, this increase is much less.
  6. Fat absorption test taken orally.
  7. Serum turbidity test. It is based on the assessment of serum turbidity after oral administration of vegetable oil (in the dose 5 ml / kg m.c.). Serum is assessed three times at one hour intervals after fat administration. If there is no turbidity of the serum (due to hyperlipidaemia) within the 2 hour after feeding, it is likely that you have a TSS or malabsorption syndrome. In such a situation, the diagnosis can be confirmed by administering the oil together with a preparation containing pancreatic enzymes. In the case of ZNT, it will be noticeable in the second hour pronounced hyperlipidemia.

Most of these tests are outdated and not performed now, especially since the available and relatively inexpensive is very sensitive and specific cTLI test.

Differential diagnosis

Primary or secondary causes of small intestinal diarrhea.

Weight loss disorders (e.g. systemic diseases, diabetes, liver failure, malignant tumors and others).

Patients with disturbed pancreatic duct or those who are deficient in enteropeptidase in the small intestine have the same clinical signs that are also classified as EPI, although dogs do not lack pancreatic enzymes.

A subclinical form of pancreatic insufficiency in a dog

Let us return for a moment to the pancreas itself and its functional reserve.

It has been said that this organ manifests its symptoms of hypothyroidism very late and it is only when the digestive part is almost completely destroyed that it lets you know loudly and emphatically about its ailment.

The functional reserve of the pancreas is therefore a "double-edged" weapon:

on the one hand, it is great that our heroine is so tough and strong, because it enables proper digestion and absorption of food for a long time after the destruction of acinar cells begins.

On the other hand, maybe it would be better if the pancreas gave notice a little earlier, before the organ is almost completely destroyed?

This would give us a chance to support its functions, provide dietary supplies and monitor the development of the disease

In any case, sometimes it is possible to "capture" the moment of mild reduction of pancreatic function in clinically healthy dogs, not showing any symptoms yet.

Then such a disorder is called subclinical exocrine pancreatic insufficiency.

It is suspected that it indicates the partial atrophy of acinar cells.

Statement form of subclinical pancreatic insufficiency is based on obtaining results from the so-called. gray zone - that is, in the range between 2.5 and 5 μg / l.

One abnormal result does not prejudge anything and does not allow for the diagnosis of subclinical TSD.

It is important not to treat such findings as developing full-blown CTS.

The duration of the latent disease stage is highly variable and some dogs never develop symptoms of overt exocrine insufficiency.

Additional testing should be performed in dogs that achieve breakpoints for cTLI after fasting.

It is recommended to perform a cTLI test before and after pancreatic stimulation, i.e. after administration of a meal.

An alternative may be endogenous stimulation of the pancreas by intravenous administration cholecystokinin and secrets.

The confirmation of the diagnosis of TSF is the lack of response to pancreatic stimulation.

Dogs with subclinical disease generally have low fasting cTLI values, but the fed test results are normal.

Secondary and accompanying ATD diseases

Unfortunately, pancreatic insufficiency always echoes throughout the body.

It is very often accompanied by various types of disorders as a result of impaired digestion and absorption of nutrients.

Sometimes comorbidities have nothing to do with enzyme deficiency, yet they are reported to be higher in patients with TSD.

It is important to realize that the disease is not just about diarrhea and emaciation.

It is also:

  • mineral and vitamin deficiencies,
  • predisposition to infections within the gastrointestinal tract,
  • decrease in immunity,
  • many other.

The most common abnormalities that coexist with TST include:

An overgrowth of bacterial flora in the small intestine

In the case of pancreatic enzyme deficiencies, it often occurs excessive multiplication of microorganisms in the intestines.

This is for a number of reasons.

First of all - undigested food debris in the lumen of the intestines is a fantastic source of substrates for bacteria.

The microorganisms are thus provided with enough ingredients to be able to multiply quickly.

The overgrowth of flora is favorable gastrointestinal motility disorders, and due to the fact that the secretion of the pancreas additionally has a bacteriostatic effect, the mechanisms protecting against "invasion " of bacteria are reduced.

All these factors lead to the phenomenon known as SIBO (small intestinal bacterial overgrowth).

Some people refer to it as antibiotic-responsive diarrhea.

SIBO rarely develops in dogs with a subclinical form of NNT.

How to state that there has been an excessive multiplication of microorganisms?

In this case, as a rule, it comes to increase in the concentration of folic acid in the blood serum and decrease in cobalamin levels, that is vitamin B12.

Folic acid is an intermediate of bacterial metabolism; bacteria synthesize its increased amount and it is then absorbed by the appropriate receptors of the anterior segment of the small intestines.

As a result, its level in blood serum increases.

Cobalamin is a water-soluble vitamin, involved in many biochemical reactions.

The diet of the belts is rich in vitamin B12, therefore - with proper digestion and absorption - we rarely deal with its deficiency resulting from the lack of food.

However, in the course of TSD, the absorption of cobalamin from the gastrointestinal tract is reduced, which results in its deficiency in the body.

The population of bacteria that live in the gut has a huge impact on intestinal mucosa.

The overgrowth of anaerobic bacteria leads to partial atrophy of the intestinal villi and reducing the activity of brush border enzymes.

Aerobic overgrowth, on the other hand, does not have such consequences.

In many cases, there is no need to treat SIBO - often the mere administration of pancreatic enzymes is sufficient for the clinical symptoms to begin to regress.

However, if the expected improvement does not appear, SIBO can be treated with antibiotics for approx 1-3, sometimes even up to 12 weeks:

  • tylosin - 20 mg / kg m.c. orally every 8-12 hours,
  • metronidazole - 10-20 mg / kg m.c. orally every 8 hours,
  • oxytetracycline 10-20 mg / kg m.c. orally every 8 hours.

Cobalamin deficiency

Vitamin B12 deficiency results from the lack of production of an endogenous factor by acinar cells in the pancreas.

Due to the fact that it is species-specific, it cannot be replaced after the introduction of pancreatic enzyme supplementation.

Therefore, in the presence of a deficiency of cobalamin, supplementation is recommended.

Initially feeding cyanocobalamin parenterally (as a subcutaneous injection at a dose of 250-1200 μg / dog once a week for 4-6 weeks, then once every two weeks for 4-6 weeks, then once a month.

Thereafter, the frequency of administration is determined by re-measuring the serum cobalamin concentration (30 days after the last injection).

It is noteworthy that the average survival of dogs with the concentration of vitamin. B12> 100 ng / l is twice as high as in patients who did not receive cobalamin and its concentration is < 100 ng/l.

Torsion of the mesentery

It does not have a causal relationship with NNT, however, it is a disorder that is often observed in patients with this disease.

Less common diseases appearing in dogs with endocrine pancreatic dysfunction, or rather not causally related to TSD, include:

  • skin diseases,
  • diseases of the musculoskeletal system,
  • gastrointestinal diseases not related to TSD,
  • neuromuscular diseases,
  • diseases of the genitourinary system,
  • cardiovascular and respiratory diseases,
  • diabetes.

Treatment of dog pancreatic insufficiency

Outpatient medical care should be directed to supplementation of digestive enzymes and cobalamin (if necessary).

Inpatient care is usually for diabetic patients and is based on insulin therapy.

Pancreatic insufficiency in dogs

Pancreatic insufficiency in dogs

Supplementing the deficiency of pancreatic enzymes

The treatment of choice, regardless of the cause of exocrine pancreatic insufficiency, is to provide digestive enzymes with each meal.

Most preparations containing pancreatic enzymes are obtained from pork pancreas.

They contain lipase, amylase, protease and digest fats, carbohydrates and proteins, respectively.

Veterinary products are available in powdered form as uncoated tablets (Viokase-V, Pancreazyme), unfortunately - many veterinary drugs are not registered in Poland.

Medicines available in human medicine are in the form of capsules (creon 10000) or coated tablets (Neo-Pancreatinum).

Simple extracts of pork or bovine pancreas (e.g. Pancreatin), preferably in powdered form, mixed with each meal mixed with enzymes immediately before serving (usually 1 teaspoon / 10 kg m.c.).

The dose may be reduced after a response is obtained.

The enzyme activity may vary depending on the product.

Raw pancreas and powdered preparations containing digestive enzymes are the most effective.

Uncoated tablets can be crushed, thereby increasing their effectiveness.

However, coated enteric-coated tablets if capsules are not recommended for use.

Enzymes closed in this form are protected against gastric acid until the protective layer is removed.

For this you need bicarbonate, which is produced by the pancreas, so using this form of enzymes simply misses the point.

In turn, the addition bicarbonates is not recommended as such an action stimulates the production of stomach acid.

Complex pancreatic extracts containing bile salt supplements (Pancreatan comp., Pancreon comp.).

An alternative to tablets, capsules and powders may be feeding raw bovine or pork pancreas.

Oral dose per meal for a dog weighing approx 20-35 kg this 50-100 g.

Preparations containing acid-resistant fungal lipase (Combizym, Pancreolan).

If the patient has a cobalamin deficiency, it should be supplemented:

  • it must be administered parenterally (usually by subcutaneous injection),
  • pure cyanocobalamin should be used,
  • the dose is 250 to 1,200 μg per injection, depending on the size of the dog. Some dogs only need short term cobalamin supplementation. Others require lifelong administration.

Antibacterial drugs

Antimicrobials are considered in patients who are unresponsive to enzyme replacement therapy and cobalamin supplementation.

They can be used in treatment small intestine dysbiosis (however, this usually does not require antibacterial therapy and usually resolves after starting treatment).


Treatment reduces the pH of the stomach. It is used omeprazole 0.6 mg.kg m.c. every 12 hours.

Vitamin E and K

Serving is recommendable vitamin E at a dose of 5-8 j.m. orally once a day and vitamin K 1-2 mg / kg m.c. (subcutaneously).

Other medications depend on diagnosed comorbid conditions in patients who do not respond to initial therapy.

Research has been conducted on alternative sources of pancreatic enzymes, but the considerable costs and limited availability of these substances make their use practically impossible.

It is a pity, because enzymes of bacterial origin (because we are talking about them) seem ideal for the treatment of PTS.

Bacterial lipase, obtained from Burkholderia plantarii bacteria is more effective in eliminating the symptom of fat in the stool than pig pancreatic enzymes.

It passes unchanged through the stomach and intestines and can be used in a much smaller dose.

Similarly fungal lipase, derived from the fungi of the genus Aspergillus, it is acid-resistant - it is not destroyed when passing through the stomach.

On the other hand, it is inactivated by proteases and bile acids in the small intestine, which makes it less effective than traditional enzyme sources.

Treatment of subclinical NNT

Treatment of canine pancreatic insufficiency Treatment of dogs with subclinical exogenous pancreatic insufficiency is not necessary.

Hopes were associated with the immunosuppressive treatment of cases of probable atrophy of acinar cells in order to avoid the development of clinical TSF, however, the use of immunosuppressants is not recommended due to the unforeseeable pace of disease progression from its latent to overt form.

What if the improvement you get for your dog is small?

You can try to increase the effectiveness of enzymes in several ways:

  1. Increase the dose of enzymes until a satisfactory effect is achieved (reduction of the volume of stools and frequency of bowel movements).
  2. Introduce enzymes in a different form (if uncoated tablets were used, try to crush them first or introduce powder or raw pancreas).
  3. Incubate the food after mixing with enzymes for 20-30 minutes before feeding.
  4. Concomitant administration of H2 receptor antagonists. Such drugs as cimetidine if famotidine, reduce the acidity of the stomach contents, thanks to which more enzymes have a chance to reach their destination, i.e. the intestines. This approach may be introduced from the time of initiation of enzyme therapy or reserved only for patients who respond poorly to enzyme therapy. Action antihistaminics allows you to reduce the doses of pancreatic enzymes by up to 50%. If their administration is justified, it makes it possible significant reduction of treatment costs. However, pre-incubating food with the enzyme or adding antacids or bile acids are not always necessary. Many patients respond well to standard medication without the need for supportive treatment.
  5. Addition of bile salts. Administration of alkalizing substances such as sodium bicarbonate, magnesium and aluminum hydroxide. The usefulness of these methods is controversial as they may have side effects, e.g. inhibit the secretion of bile enzymes.

Side effects of enzyme administration

Administration of enzymes in high doses may cause gastrointestinal dysfunction, e.g.:

  • diarrhea,
  • intestinal cramps,
  • nausea.

Some dogs may develop ulcers and bleeding from the mouth, which is most likely the result of digestive enzymes coming into contact with the mucosa.

Ulceration can be minimized and bleeding to stop can be resolved by reducing the doses of enzymes or by incubating them for longer with food before feeding.

Strong body odor has been anecdotally reported in some dogs supplemented with enzymes.

Pancreatic insufficiency in the dog's diet

As a rule, a slight change or modification of the diet can alleviate clinical symptoms, however there is no only proven way of eating.

It is selected on the basis of the so-called trial and error.

In contrast to ZNT in humans, where is recommended high fat diet (to maximize weight gain), in dogs this nutrition may increase the severity of diarrhea and thus the need for pancreatic enzymes.

Therefore, in most cases it is recommended use of feeds with a moderate fat content.

It is also recommended to replace a diet rich in large amounts long-chain fatty acids on the one in which they dominate medium chain fatty acids.

Such modification may not alleviate clinical symptoms, but may increase the degree of intestinal absorption of cholesterol and fat-soluble vitamins, which in dogs with EPI is very limited.

The composition of the optimal feed should include:

  • larger share good quality protein,
  • normal carbohydrate content but limited simple sugars.

However, diets rich in dietary fiber are not recommended, because they are less digestible, they increase the volume of the faeces and can interfere with the absorption of other nutrients.

However, there are situations in which the consistency of the stool is improved and flatulence is reduced when eating a diet rich in fiber.

Foods containing hydrolyzed protein - they lead to the improvement of the body condition in animals with TSD.

As a general rule, when starting treatment, you should introduce an easily digestible diet in combination with enzyme supplementation.

Serving meals 2 times a day as a rule, it is quite enough.

Avoid extremes - high or low fat diets as well as high fiber diets.

In the absence of response to such therapy, the dose of pancreatic enzymes is initially titrated before attempting to change nutrition.

Treat dogs should be avoided (at least initially) until clinical signs are under control.

Support diet

Chopped bovine, pork, lamb or game pancreas can be stored frozen for months without losing enzyme activity.

They should be replenished with approximately 30 g / 10 kg m.c.

Enzyme supplementation can overcome food aversion or food allergy.

But be careful!

There is some risk of transmission of Echinococcus multiocularis from game pancreas.

Similarly, there is a theoretical risk of transmission of bovine spongiform encephalopathy or Aujeszky's disease from pigs.

However, it is not higher than when using powdered products.

Monitoring a sick dog

What do we expect from the introduction of treatment?

With optimal treatment and adherence to dietary recommendations, we expect rapid weight gain of our emaciated patient.

It should be remembered that body weight may not fully return to normal despite remission of clinical symptoms.

In uncomplicated cases diarrhea usually resolves within 2-7 days.

Regular check-ups are necessary in dogs diagnosed with exocrine pancreatic insufficiency.

The patient's condition should be assessed on 2-4 weeks after the initiation of treatment and after any changes to it.

The most important prognostic factors are:

  • weight gain,
  • appetite,
  • improvement in condition.

The owner should pay particular attention to any changes in the consistency and volume of the stool and inform the attending veterinarian about it.

For patients who respond very well to treatment, follow-up visits may be once or twice a year (as in healthy adult dogs).

Side effects of therapy

As is the case with virtually all diseases and their treatment, also here some "side effects " of the therapy may appear:

  1. You may become reluctant to eat due to the addition of enzymes. It is quite rare in dogs.
  2. About 20% of patients do not respond to the initial addition of enzymes.

Prompt diagnosis and treatment may also require:

  • parallel cobalamin deficiency,
  • small intestine dysbiosis,
  • inflammatory bowel disease,
  • diabetes or other conditions.

Dog pancreatic insufficiency and prognosis

Dog pancreatic insufficiency and prognosis

Exocrine pancreatic insufficiency is a lifelong disease in almost all patients (only isolated cases of recovery are documented) and the necessity should be accepted lifetime treatment.

As a rule, improvement is observed within a few weeks after the introduction of therapy, and then stabilization of the patient's condition.

The prognosis for most dogs is beneficial, and the response to long-term enzyme therapy after stabilization of the acute condition is good.

Of course, there may be occasional brief relapses and exacerbations, but these are manageable quickly.

Generally dogs can lead a normal life and attain a normal life span.

However, it happens that some patients do not respond adequately to therapy

Unfortunately, approximately 20% of patients with TSD are euthanized for lack of clinical improvement and / or medical costs.

Parallel cobalamin deficiency is recognized as bad symptom and needs to be treated.


There is currently no way to prevent the occurrence of EPI.

Due to the genetic background of the disease in some breeds, patients with known exocrine pancreatic insufficiency should not be used for breeding.


What is associated with exocrine pancreatic insufficiency?

In most cases, dogs with NNT will require lifelong treatment, and depending on the size of the patient - it can be costly.

There are family predispositions and the family nature of the disease (German shepherds, collie).

Development is possible diabetes in breeds other than German Shepherds.

So far, little is known about the pathogenesis and progress of the disease from the subclinical to the clinical phase. Research directed at this can help slow it down or even prevent it disease development in the classified phase.

Currently, the diagnosis of exocrine pancreatic insufficiency is not a problem for veterinarians, and treatment in most cases brings good results.

Enzymes should be supplemented on a permanent basis until the end of the animal's life, and the effects of treatment and obtaining a quick clinical improvement largely depend on the discipline of the animal caregiver.

At first, monitoring meals and administering enzymes may seem laborious, however, it quickly becomes "routine" and the owner has to watch how the emaciated pooch finally takes shape and ceases to focus solely on searching for food.

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