Complex therapy of insufficiency of exocrine pancreatic function in dogs. Factors causing pancreatitis

Canine pancreas diseases

The pancreas is located between the layers of the mesentery of the duodenum and the stomach, and has a right and left lobe. Her excretory ducts open at duodenum. The mass of the gland is 10-100 g, which corresponds to 0.13-0.36% of the dog’s body weight. The endocrine part of the gland makes up only 3% and is formed by cells of the islets of Langerhans. Alpha cells secrete the hormone glucagon, beta cells secrete insulin. In addition, this part of the gland produces lipocaine, vagotonin and other hormone-like substances.

Most of the gland has exocrine function and produces digestive juice containing enzymes trypsinogens, chymotrypsinogens, proelastase, ribonuclease, amylase, lipase, which are involved in the digestion of proteins, carbohydrates and fats supplied with food. Due to the fact that most of glands are an exocrine organ; with the development of a pathological process, the digestive function primarily suffers. Only in chronic disease is the insular part involved (or in the case of its specific lesion). Then it is violated endocrine function glands.

Four main forms of pancreatic damage have been described: acute pancreatitis, chronic sclerosing pancreatitis (pancreatic cirrhosis), hereditary atrophy and insulinoma. Insulinoma and atrophy occur in German Shepherds, in isolated cases in hounds and giant schnauzers. In dogs of other breeds, chronic sclerosing pancreatitis is predominantly found, manifested more often by symptoms of diabetes than exocrine insufficiency. Similar selectivity in occurrence acute pancreatitis No. The incidence of pancreopathy in German Shepherds is 8 per 1000, and in other breeds - 3 per 10,000

Exocrine insufficiency . The pancreas, due to its complex anatomical localization, is difficult to treat with conventional physical methods research. Its condition can only be judged by the dysfunction of other organs associated with it. Insufficiency of gland function can manifest itself both in a lack of enzymes and in the inability of digestive juice to maintain an alkaline pH in the intestines. Under these conditions, normal intestinal cavity digestion is disrupted, microbes multiply intensively in the small part, and intestinal dysbiosis occurs, which further worsens digestive processes. Parietal enzymatic digestion (maldigestion syndrome) and absorption of enzymatic hydrolysis products (malabsorption syndrome) are disrupted. Exhaustion increases with increased appetite(malnutrition syndrome), the function of other endocrine glands is disrupted.

Symptoms. Endocrine pancreatic insufficiency is characterized by: polydipsia and polyuria, vomiting, flatulence (discharge of foul-smelling gases), pancreatogenic diarrhea (smelly, with frequent bowel movements and an increase in the volume of feces, not amenable to therapy), pancreatogenic stool (polyfecal - bulky stool in the form of foamy, soft, spongy colorless masses with sour smell, greasy sheen and undigested food debris, sometimes mixed with blood), polyphagia up to coprophagia, flatulence in all parts of the intestine, hyperglycemia, glucosuria, hypocholesterolemia, increased amylase levels in the blood serum, steatorrhea, creatorrhea, amilorrhea, acidification of feces.

Diagnosis It is not always possible to install it during the animal’s lifetime. If the listed symptoms are detected during examination, there is reason to suspect pancreaopathy. Ascites in combination with hyperglycemia also indicates the participation of the pancreas in the pathological process. To be more confident in making a diagnosis, one or two functional tests are performed.

Differential diagnosis. Symptoms of exocrine pancreatic insufficiency must be distinguished from polyphagia caused by chronic enteritis, and various types malabsorption. For pancreopathy characterized by polyphagia against the background of progressive cachexia. Animal activity and performance for a long time may persist, which is not typical for chronic enteritis and hepatopathy (rapid increase in depression, temporary or long-term loss of appetite). Pancreaopathy is also distinguished by concomitant bradycardia; in contrast to enterocolitis, defecation is frequent, but there is no tenesmus.

Acute pancreatitis . Necrosis of the pancreas caused by enzymatic autolysis of tissues with hemorrhagic impregnation of them. The etiology is not precisely established. Acute pancreatitis occurs when bile enters the lumen of the gland ducts. Important role plays the activation of proteolytic enzymes in the gland itself, resulting in enzymatic digestion (autolysis) of its parenchyma with hemorrhages and fatty necrosis.

Symptoms. Acute pancreatitis occurs more often in females with impaired fat metabolism. The disease begins suddenly after eating and develops over several hours or days. In mild cases, the primary concern is increasing weakness, apathy, vomiting, foul diarrhea, increased body temperature, sometimes anemia, jaundice, ascites and other symptoms of exocrine pancreatic insufficiency syndrome.

Severe cases of the disease ( acute necrosis pancreas) are manifested by severe pain, quickly leading to the development of collapse and shock. The pain is accompanied by painful vomiting, salivation and bradycardia. The animal takes a forced “praying” pose: the front legs are extended forward, the chest lies on the floor, and rear end body is raised. Palpation reveals acute pain abdominal wall. In the blood and urine, already in the first hours of the disease, increased content amylase. However, with necrotizing pancreatitis, the amylase content may be normal or even reduced. In these cases, a certain diagnostic value have a decrease in the amount of calcium in the blood and an increase in aspartate aminotransferase activity.

Acute pancreatitis lasts several days and may result in complete recovery or develop into chronic recurrent pancreatitis. In severe forms, death can occur in the initial period of the disease with symptoms of collapse, shock and peritonitis.

Treatment provides: 1) combating shock - intravenous drip infusion of a 5% solution of glucose, dextrans, blood or plasma transfusion; 2) creation of physiological rest for the pancreas: complete fasting for 2-4 days, subject to parenteral administration of alvesin; 3) inactivation of proteolytic enzymes with antienzyme drugs (Gordox, Contrical, etc.); 4) suppression of pancreatic secretion and elimination of pain (atropine and analgin with seduxen); 5) prevention of secondary infection (antibiotics).

If acute pancreatitis is suspected, it is better to play it safe and immediately begin intensive treatment, since in case diagnostic error it will not harm, and delay in prescribing therapy will no longer save the patient’s life. When the animal's condition improves, it is recommended to slowly begin feeding high-quality proteins and fat - several times a day in small portions.

Pancreatic atrophy . The atrophied gland looks no thicker than a parchment sheet, is transparent, but retains its ducts. Mostly German Shepherds are affected. The etiopathogenesis is unknown. Animals are born with a normal pancreas. Its atrophy and, as a consequence, exocrine insufficiency develop in the first months of life, but sometimes in middle age. The factors causing gland atrophy have not been established.

Symptoms. A history of the disease is characteristic, indicating extreme hunger of the animal to the point of eating its own feces and, despite this, progressive emaciation. Along with general symptoms insufficiency of gland function, the semiotics of the disease is supplemented by the following data: defecation is frequent, the number of feces is very increased, they are excreted in large single or multiple small scattered heaps, have a wet sheen, foamy consistency, with an unpleasant sour odor and, depending on the fat content in them, colorless gray or clay-yellow. In such pancreatogenic stool you can find undigested grains of cereals or pieces of potatoes. At times, feces may be shaped. The sounds of splashing and rumbling are auscultated in the abdominal cavity, and the large intestine filled with fecal matter is palpated. Bradycardia is pronounced. The coat of a sick animal is disheveled, does not adhere well, dry skin, scaly.

Diagnosis diagnosed almost unmistakably by a combination of five symptoms: German Shepherd, severe emaciation of the animal, insatiable appetite, pancreatogenic stool, hypocholesterolemia.

Atrophic pancreatitis completely eliminates the reserve secretory ability of the gland. Without treatment, sick animals die.

Treatment. The main role is given to replacement therapy. The animal is prescribed pancreatic enzyme preparations (Pancreatin, Panzinorm), painkillers and antibiotics. Diet. It is recommended to feed only lean meat and no fats or carbohydrates. If treatment is ineffective, euthanasia is offered.

Insulinoma . Hormonally active tumor, adenoma, developing from beta cells of the islets of Langerhans, producing excess quantity insulin. It is very rare in German Shepherds. Excessive production of insulin by adenoma causes increased destruction of glucose in the body and a state of chronic hypoglycemia.

Symptoms. Hypoglycemia leads to muscle tremors, ataxia, epileptiform seizures and, in the final stage, hypoglycemic coma.

Diagnosis suggested based on three signs: German Shepherd, hypoglycemia below 2.8 mmol/l, epileptiform seizures. Differentiate from severe liver dystrophy and insufficiency of adrenal cortex function. Final confirmation of the diagnosis can only be done by diagnostic laparotomy.

Treatment. If insulinoma is detected, a partial pancreaectomy is performed. Before surgery, therapeutic diet: 1/3 meat and 2/3 starch jelly, 4-6 servings per day.

Operation technique. General anesthesia is performed in the dorsal position of the animal, and then a laparotomy is performed along the white line in the supra-umbilical region. Organs are examined. The lobe of the gland affected by the tumor is isolated. The glandular tissue is separated using tweezers at some distance from the tumor and the intralobular artery is exposed. The arteries are ligated and divided. The affected part of the gland is removed. The abdominal wall wound is sutured.

Most common cause development of exocrine pancreatic insufficiency (EPI) in dogs is atrophy of the secretory acini in the pancreas. Most often this pathology is detected in German shepherds, but the disease can develop in dogs of other breeds, including mixed breeds. German Shepherds are known to have a genetic predisposition to NEFP, but the etiology of this phenomenon is unknown. The disease is progressive: at a young age, the exocrine function of the pancreas is normal; the first clinical signs of the disease begin to appear in animals aged 1 to 5 years. In other cases, NEFP may be caused by chronic, recurrent inflammation (pancreatitis), as commonly seen in cats, and pancreatic hypoplasia. NEFPZh and diabetes often complicate the course of chronic pancreatitis in dogs.

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2.1 Pathophysiology

Clinical signs of NEFP usually appear when the secretory activity of this organ is reduced by approximately 90%. Insufficiency of digestive enzymes leads to disruption of the processes of digestion and absorption in the intestines. In addition, abnormal activity of digestive enzymes in small intestine, traffic violation nutrients, atrophy of intestinal villi, infiltration of intestinal mucosa with inflammatory mediator cells were established in all cases of NEFP. A common complication accompanying the disease is a violation of the intestinal microflora, which often leads to enteropathies caused by taking antibiotics (EPA).TABLE OF CONTENTS

2.2 Clinical symptoms and results of general physical examination

The three classic signs of NEFP are chronic unexplained diarrhea, weight loss, and polyphagia. In this case, feces are poorly formed and are excreted in large quantities and have signs of steatorrhea. Often observed loose stool. Sick animals often have a tendency to coprophagia, and vomiting is rare. Dog owners celebrate their pets severe flatulence and rumbling in the stomach. Externally, dogs with NEFP appear emaciated, muscle mass their hair is reduced, their coat loses its shine and becomes unpleasant and greasy to the touch. However, animals are physically active and mobile. If your dog is lethargic, refuses food, and has a fever, another medical condition is likely causing the diarrhea.TABLE OF CONTENTS

2.3Diagnostics

Many laboratory tests are used to diagnose NEFP, with the most effective method- definition trypsin-like immunoreactivity (TPIR) in the blood. Kits for determining TPIR are strictly species-specific, so only special kits should be used for dogs and cats (for example, a kit is used for catsfTLI from GI-Lab , USA). Other laboratory research(biochemical or hematological) do not give a specific result, but they are necessary to identify concomitant diseases. If helminth infestation or bacterial contamination is suspected, feces are examined (for the presence of helminth eggs and for bacteriological cultivation).

TPIR measures the amount of trypsinogen in the patient's blood. The only source of trypsinogen in the body is the pancreas, so the test result indirectly reflects the amount of functionally active glandular tissue. The determination of TPIR is carried out after a 12-hour fast and is very sensitive and specific. Values ​​below 2.5 µg/l clearly indicate NEFP, while values ​​in the range of 2.5-5 µg/l correspond to the norm. TPIR is stable at room temperature and can remain unchanged for several days, but it quickly degrades when heated. Therefore, samples, especially in summer, should be protected from direct contact sun rays. If the content of TPIR in the patient’s blood is normal, the diagnosis of NEFP is excluded.TABLE OF CONTENTS

2.4 Treatment

Most dogs and cats with NEFP have a good clinical response to enzyme replacement therapy .Convenient In general, use powdered enzyme substitutes without special coatings. The initial dosage is 2 teaspoons of powder for every 20 kg of animal body weight with each portion of food. It must be emphasized that enzyme substitutes must enter the animal’s body with every portion of food, even with treats. Otherwise, diarrhea may return. Enzyme replacement tablets or capsules for cats and dogs are less effective than powders. The clinical symptoms of NEFP are weakened after the start of enzyme replacement therapy, and in the future the dose of enzyme replacement can be gradually reduced until minimal effective dosage. It should be kept in mind that different batches of replacement enzymes may have different enzymatic activities. When treating NEFPZh, one should not supplement enzyme replacement therapy by pre-treating the feed with enzyme preparations for 30 minutes, administer drugs that reduce the acidity of gastric juice (for example, type 2 histamine receptor antagonists) and enrich the animal’s feed with bile salts or soda. Very good substitutes for pancreatic enzymes are fresh frozen pig pancreas. When stored frozen at -20°C, they retain a large amount of active enzymes for 1 year.

For cats with NEFP, it is good to supplement enzyme replacement therapy with parenteral administration of cobalamin, since with this pathology the absorption of vitamin B 12 in the digestive tract is impaired.TABLE OF CONTENTS

3Pancreatitis

Pancreatitis in cats and dogs is difficult to diagnose, but careful examination can reveal a number of symptoms. The easiest way to identify is acute necrotizing pancreatitis, the outcome of which is usually unfavorable. Sluggish, recurrent acute or chronic pancreatitis is most common in cats and quite common in dogs. Treating pancreatitis is quite difficult. Severe acute forms require immediate hospitalization of the patient and intensive care to prevent death. At the same time, sluggish chronic pancreatitis can be treated at home with the help of appropriate diet therapy.TABLE OF CONTENTS

3.1.Definitions and pathophysiology

Pancreatitis in small domestic animals represents a variety of forms of diseases that vary in severity - from mild subclinical forms that occur without obvious symptoms to acute necrotizing pancreatitis, which most often ends in the death of the patient. The classification of forms of pancreatitis is based on histopathological changes in the tissues of the pancreas:

Acute pancreatitis: neutrophil infiltration, necrosis, edema. The changes are potentially reversible.

Chronic pancreatitis: monocyte infiltration, fibrosis. Usually has a relapsing course.

These types of disease, in turn, are divided into subtypes, including acute necrotizing pancreatitis (in which there is severe necrosis of the fatty tissue surrounding the pancreas) and active chronic pancreatitis (characterized by infiltration of the pancreatic tissue with both neutrophils and monocytes against a background of nodular pancreatic hyperplasia and fibrosis) . Histopathological classification is useful for understanding the mechanisms of disease development, but is not very useful clinically. In this regard, it is more convenient to use a classification based on the characteristics of the clinical course of the pathology, taking into account scores for the severity of pancreatitis and its symptoms (see table).

Scoring system for assessing the severity of pancreatitis in dogs and cats (according to Ruaux , 2000)

*Note: Point system Assessment of the severity of pancreatitis is based on the number of organ systems involved pathological process and damaged as a result of illness at the time of application for veterinary care.

The pathophysiology of pancreatitis is still not fully understood. Acinous cells of a healthy pancreas secrete enzymes involved in the initial stage of digestion of food components (the products of their activity, relatively low molecular weight compounds, are further destroyed by enzymes of the brush border of the cells of the small intestinal mucosa). Pancreatic enzymes include lipase (the pancreas is the main source of this enzyme), a-amylase, phospholipase, proteolytic enzymes (elastase, chymotrypsin and trypsin). Normally, pancreatic cells are protected from the effects of produced enzymes due to the fact that many of them are synthesized in the form of inactive precursors, so-called zymogens (for example, trypsinogen and chymotrypsinogen). Zymogens accumulate in special granules separated from lysosomes. In addition, the contents of the granules contain a pancreatic trypsin inhibitor, which prevents the premature activation of this enzyme. Trypsin activation occurs in the lumen of the small intestine under the action of enterokinase. The activated trypsin then activates chymotrypsin.

The main link in the pathogenesis of pancreatitis is the unacceptable fusion of lysosomes with granules containing zymogens in acinar cells of the pancreas. The acidic environment of lysosomes inactivates secreted trypsin and other enzymes in cells, causing local " self-digestion", is developing inflammatory reaction and necrosis of the acini of the pancreas, and then necrosis of the fatty tissue surrounding the pancreas. Free enzymes enter the abdominal cavity, where they cause local or extensive peritonitis, as well as into the bloodstream. In the blood, pancreatic enzymes are relatively quickly inactivated by a number of plasma protease inhibitors, in particular, α-1-antitrypsin (also known as plasma protease inhibitors). a r protease inhibitor"). Inhibitor o ^- antitrypsin temporarily binds proteases and then transfers them to a 2 -macroglobulin, which, in turn, binds these enzymes irreversibly. The resulting complex of pancreatic enzyme and o ^- macroglobulin excreted by the reticuloendothelial system. For severe pancreatitis, the number of proteinase inhibitors V blood decreases, and free active proteolytic enzymes appear in the plasma. The action of these enzymes, as well as the activation of neutrophils and monocytes, the absorption of endotoxins from the lumen of the gastrointestinal tract into the bloodstream and the release pro-inflammatory cytokines and reactive oxygen radicals directly from the tissues of the pancreas and leukocytes into the blood, alveoli and other organs lead to generalized inflammatory reaction, vasodilation, increased blood clotting and simultaneous activation of fibrinolysis. In particularly severe cases, disseminated intravascular coagulation (DIC) may occur. The functions of many organs are impaired, especially the kidneys (prerenal and/or renal azotemia develops) and lungs (in especially severe cases, pulmonary edema and acute respiratory failure may develop).

The factors leading to the development of pancreatitis in each specific case are not fully known. Under experimental conditions, it is possible to induce the development of pancreatitis by obstructing the secretory duct of the gland. In this case, the disease is usually mild, although it can be aggravated by stimulating the secretory activity of the pancreas. Obstruction of the excretory duct caused by a neoplasm in the pancreas due to cholangitis or inflammation of the intestine can cause pancreatitis. This is especially true for cats, in which the excretory duct of the pancreas merges with the bile duct at the point of entry into the duodenum.

In dogs, the development of pancreatitis is often preceded by overeating fatty foods. It is possible that in this case the pathogenetic mechanisms leading to pancreatitis begin with stomach overfilling and stimulation of increased secretion in the pancreas. An important factor contributing to the development of pancreatitis is hypertriglyceridemia(hereditary or caused by diet or endocrine disorders). Pancreatitis can also result from taking certain medications. However, regarding steroids, the data are contradictory: these drugs actually increase the activity of lipase in the secretion of the gland by 5 times, but so far in the experiment they have not been able to induce pancreatitis.TABLE OF CONTENTS

3.2 Clinical symptoms

Clinical signs of pancreatitis vary depending on the severity of the disease. The classic triad of symptoms (vomiting + severe pain in the cranial abdomen ± “praying pose”) in dogs and cats is observed only in severe, acute cases. Pancreatitis is often accompanied by acute colitis, in which fresh blood is observed in small amounts of feces - this is a consequence of local peritonitis spreading to the transverse colon, adjacent to the left lobe of the pancreas. In severe cases, the patient experiences collapse and signs of dehydration against the background of shock symptoms, and in especially severe cases, acute renal failure, respiratory failure, and disseminated intravascular coagulation syndrome.

In other, milder forms of acute or chronic pancreatitis, the symptoms of the disease may be mild. Usually it is represented by anorexia with or without mild attacks of colitis, periodic vomiting, increased flatulence and mild abdominal pain. These forms of pancreatitis are especially common in cats. In these animals it is often very difficult to distinguish pancreatitis from cholangitis or intestinal inflammation. In addition, in cats, these pathologies often accompany each other, which further complicates diagnosis.

With pancreatitis, there is a risk of developing acute or chronic complications. Acute forms diseases can cause dehydration, acidosis, disorders electrolyte balance as a consequence of transient vomiting and anorexia (hypokalemia, hypochloridemia, hyponatremia), prerenal azotemia, and in some cases, a systemic inflammatory reaction, hypotension, respiratory failure and disseminated intravascular coagulation syndrome. In cats, acute pancreatitis is often accompanied by the development of hepatic lipidosis. Pancreatitis in cats (less often in dogs) is also accompanied by cholangitis and cholangiohepatitis, which is determined by the anatomical proximity of the proximal pancreas and bile duct in both species. The liver tissue is affected due to inflammatory mediators entering it with blood from the portal vein.

Chronic pancreatitis can cause the destruction of so much of the secretory units of the pancreas that the patient develops diabetes mellitus, NEFP, or both diseases simultaneously. In people with chronic pancreatitis, diabetes mellitus usually develops earlier, which precedes the development of NEFP by several months. This is due to the fact that diabetes mellitus begins to manifest clinically with the loss of 80% of the active glandular tissue of the pancreas, and NEFP - with the loss of 90% of this tissue.TABLE OF CONTENTS

3.3 Laboratory diagnostics

Diagnosing pancreatitis is quite difficult, since at the present stage there are no specific and sensitive diagnostic methods, except for histopathological examination of pancreatic tissue biopsies obtained during surgery, during laparoscopy or posthumously. Clinical symptoms and medical history suggest the presence of pancreatitis, especially in acute cases: if a dog constantly experiences vomiting and severe pain in the anterior abdomen after overeating, there is reason to suspect acute pancreatitis. However, such symptom complex may also be a consequence of partial or complete intestinal obstruction, volvulus, intussusception or perforation of a stomach ulcer. With a milder course of pancreatitis in both cats and dogs clinical symptoms become nonspecific: similar signs are observed when various diseases gastrointestinal tract, liver, etc. For differential diagnosis further research is needed.

In the absence of biopsies, diagnosis of pancreatitis is usually based on clinicopathological tests and ultrasound examination of the pancreas. At clinical analysis blood most often reveals neutrophilic leukocytosis with a shift of the formula to the left (with severe forms- with a degenerative shift to the left). As the patient dehydrates, the hematocrit increases. Chronic pancreatitis in cats in 20-80% of cases is accompanied by mild anemia, which is rarely observed in dogs. In severe cases, the platelet count decreases due to DIC. Hypokalemia is common in both dogs and cats. It is often accompanied by hyperglycemia (glucose can even be detected in the urine) due to stress and the release of hydrocortisol, catecholamines and glucagon into the blood. But cats with suppurative pancreatitis may experience hypoglycemia. Although one of the possible causes of pancreatitis is considered hypercalcemia, the course of the disease leads to the development of mild hypocalcemia and hypomagnesemia due to saponification of fats in the adipose tissue surrounding the pancreas. With pancreatitis, very often detected hypercholesterolemia And hypertriglyceridemia in blood samples obtained during fasting. These deviations can be both a cause and a consequence of pathological processes in the pancreas. In severe acute cases, azotemia associated with prerenal renal failure and kidney damage due to dehydration and toxins. To clarify the severity of kidney damage, it is useful to determine the specific gravity of urine and examine its sediment. In the blood of patients with pancreatitis due to damage to liver cells by toxins entering this organ through portal vein, liver enzyme activity is often slightly or moderately increased.

The above changes are nonspecific. Monitoring these indicators is useful for assessing the effectiveness of therapy for pancreatitis, but not for diagnostic purposes. To diagnose the disease, the activity of pancreatic enzymes: amylase, lipase and trypsin is determined in the patient’s blood. For amylase and lipase, a direct catalytic determination is carried out, assessing the number of active centers, and for trypsin, a determination trypsin-like immunoreactivity (TPIR). Sometimes the content of specific pancreatic lipase (SPL) is also analyzed. This enzyme is determined immunologically by antigens that are not part of its active center. Immunological methods convenient in that they allow us to identify not only active forms enzymes, but also the corresponding zymogens. All immunological tests are strictly species specific.

In dogs, determining the level of pancreatic enzymes in the blood is the main method for diagnosing the disease. These tests are not always sufficiently sensitive and specific, but they are the most accessible and common. It would be ideal to supplement the obtained data with ultrasound examination of the pancreas. The content of pancreatic enzymes in the blood of dogs that corresponds to the norm does not exclude the presence of pancreatitis! The level of amylase rarely increases in comparison with the level of lipase and TPIR in pancreatitis, therefore, during a diagnostic study, it is not enough to determine the level of amylase in the blood only. When diagnosing the disease, the level of all three pancreatic enzymes in the patient’s blood should be determined.

In cats, methods for determining the levels of amylase and lipase in the blood have no diagnostic value. The TPIR test is the only test available to diagnose pancreatitis in cats. The specificity of the TPIR test for pancreatitis in cats is about 80%, and the sensitivity of the test is 46-80%. This is much higher than other diagnostic methods that do not involve obtaining pancreatic tissue samples.

It is optimal, however, to supplement the determination of TPIR in cats with ultrasound examination of the pancreas. Ultrasound diagnostics are good at identifying acute necrotizing forms of pancreatitis, in which enzyme production is weakened, and the determination of TPIR is especially convenient for diagnosing chronic pancreatitis, when changes in the pancreas are not noticeable during ultrasound examination.

Other diagnostic techniques are currently used in humans, dogs and cats only to clarify the diagnosis and predict the outcome of pancreatitis. They include definition trypsin-activating peptide (TPA) in urine and blood serum, the content of trypsin complex in the bloodά 1 -inhibitor proteinase and pancreatic lipase immunoreactivity (PLI) in dogs. In medicine, the content of the series is also determined pro-inflammatory cytokines in the blood serum, which makes it possible to clarify the prognosis of the outcome of the disease.TABLE OF CONTENTS

3.4 Instrumental diagnostics

Along with determining the content of pancreatic enzymes in the patient’s blood ultrasonography(ultrasound) of the pancreas is one of the few specific methods diagnosis of pancreatitis. However, the location of the pancreas in dogs and cats places increased demands on the qualifications and experience of the specialist conducting the examination. Ultrasound makes it possible to diagnose pancreatitis because this pathology is accompanied by edema of the gland, its swelling, necrosis of the adipose tissue surrounding the gland, and peritonitis. Using ultrasound, you can also identify neoplasms, abscesses or pseudocysts in the pancreas, as well as diagnose cholangitis and thickening of the walls of the small intestine near the gland.

Radiography abdominal cavity It only allows you to clarify the diagnosis of pancreatitis. It can be used to identify whether a patient has foreign bodies V gastrointestinal tract, which can be important for differential diagnosis. For acute pancreatitis in cats and dogs radiographically a decrease in density and local peritonitis in the anterior abdominal cavity is detected. The ventrodorsal projection reveals dilatation of the duodenum and its displacement lateral and dorsal to the normal position, caused by swelling of the pancreas. The transverse colon also moves, most often in a caudal direction. Contrasting It is better not to use barium: it does not provide significant advantages, and filling the lumen of the gastrointestinal tract with a contrast agent stimulates the secretion of pancreatic enzymes in the affected pancreas.. TABLE OF CONTENTS

3.5 Treatment

The method of treating pancreatitis in dogs and cats is largely determined by its form and severity at the time of seeking veterinary help. If the cause of pancreatitis can be identified (for example, hypercalcemia), it should be eliminated. In most cases, pancreatitis is idiopathic character, and only symptomatic therapy is possible. In addition, it is necessary to identify and treat concomitant pathologies that complicate the course of the disease (cholangitis, intestinal inflammation, in cats - liver lipidosis).

With severe necrotizing pancreatitis (3-4 points) in cats and dogs, the prognosis for the outcome of the disease is very unfavorable. Typically, such patients are severely impaired water-electrolyte balance against the background of a systemic inflammatory reaction, there is renal failure and increased risk DIC syndrome. Patients are indicated for intensive therapy, including blood plasma transfusions and tube feeding (in some cases, a complete transfer to parenteral nutrition). It is best to hospitalize the patient in a specialized veterinary clinic. The prognosis for the outcome of the disease is very unfavorable.

Mild forms of pancreatitis (score 0) may require hospitalization for 12-24 hours for intravenous fluid therapy, especially if the patient is vomiting and there are signs of dehydration. If there are no signs of dehydration, and general state the animal is satisfactory, it can be treated at home using the method of “unloading” the pancreas (enteral administration of fluids) for 24-48 hours. If necessary, the animal is given analgesics. For a long time, the animal is fed an appropriate diet. In animals with chronic pancreatitis Mild gastrointestinal symptoms and anorexia are usually observed periodically.

Moderate forms of pancreatitis (1-2 points), accompanied by vomiting and dehydration, require hospitalization, during which patients undergo fluid therapy, fasting treatment and pain relief. In many cases, the use of antibiotics is indicated, and in some cases, blood plasma transfusion is indicated. .TABLE OF CONTENTS

3.5.1 Intravenous administration of fluids and electrolytes

Intravenous fluid therapy is important for any form of pancreatitis, but is especially effective for milder forms of the disease. It eliminates fluid and electrolyte imbalance caused by vomiting and ensures sufficient blood flow through the pancreas. Fluid therapy uses solutions of blood substitutes (in particular, lactated Ringer's solution). The rate of administration and the volume of fluid infused depend on the degree of dehydration of the patient. For mild or moderate pancreatitis (0-1 points), a maintenance rate of fluid administration is usually sufficient. in more severe forms of the disease, it is necessary to combat developing shock (infusion rate up to 90 ml/kg/hour for 30-60 minutes). In such cases, after therapy with Ringer's solution, it is necessary to administer solutions of synthetic colloids. The content of electrolytes in the patient's blood should be closely monitored Severe pancreatitis is usually accompanied by hyponatremia, hypochloremia, hypocalcemia and hypomagnesemia, while hypokalemia is particularly dangerous and requires immediate correction. Blood potassium levels should be measured and additional potassium chloride added to the infused fluid as needed. Intravenous fluid therapy in the setting of fasting and increased renal potassium loss may worsen hypokalemia by increasing renal excretion and decreasing absorption. Given this phenomenon, it is recommended to increase the amount of potassium in lactated Ringer's solution from the usual 5 mEq/L to 20 mEq/L. The rate of introduction of potassium into the body, as a rule, should not exceed 0.5 mEq/l/kg/hour.

In especially severe cases (2-4 points), blood plasma transfusion is recommended. This allows you to replenish your reserves o^ - A ntitrypsin and (x2-macroglobulin in the patient’s blood. Blood clotting factors are introduced with donor plasma, therefore, to reduce the risk of DIC, it is better to supplement plasma transfusion with heparin.TABLE OF CONTENTS

3.5.2 "Unloading" of the pancreas

“Unloading” of the pancreas occurs during complete fasting and is traditionally used in the treatment of acute pancreatitis. When “unloading”, stimulation of the pancreas caused by filling the stomach or the entry of proteins and fats into the lumen of the duodenum is minimized. However, this technique is excluded for the treatment of people and animals with signs of malnutrition and exhaustion. Moreover, even with normal weight animals, this approach is not always acceptable - in cats, for example, anorexia Painkillers and anti-inflammatory drugs

Pancreatitis in both humans and animals is accompanied by severe pain. Patients in the clinic should be closely monitored and pain relief administered if necessary. Opiates are often used for this - morphine and its analogues (in particular, buprenorphine). Non-steroidal anti-inflammatory drugs are contraindicated for pancreatitis - their use increases the risk of ulceration in the gastrointestinal tract and potentiates the development of renal failure in animals with arterial hypertension and shock. Steroids should not be used for pancreatitis - it has not been proven that these agents reduce inflammation in the pancreas, but it is well known that steroids reduce the activity of the reticuloendothelial system. .TABLE OF CONTENTS

3.5.4 Antibiotics

With pancreatitis, infectious complications are relatively rare, but if they occur, they are very severe. In these cases, the use of antibiotics significantly reduces mortality. Therefore, broad-spectrum antibiotics are recommended for patients with acute pancreatitis, since it is not always possible to assess the risk of sepsis. For antibiotic therapy enrofloxacin and trimethoprim sulfate, which penetrate the pancreatic tissue and are effective against most pathogenic bacteria. Metronidazole is added to patients who have concomitant inflammation of the large intestine and bacterial overgrowth in the small intestine. This drug (in combination with ampicillin) is also effective for cholangitis. .TABLE OF CONTENTS

3.5.5 Antiemetics and prevention of ulceration in the gastrointestinal tract

Antiemetics help stop the uncontrollable vomiting that often occurs in patients with pancreatitis. In this case good effect(especially in dogs) gives the use of metoclopramide. However, this drug stimulates gastric motility, which in some animals increases pain and increases the production of pancreatic enzymes. In such cases, you should use Antiemetic drugs from the group of phenothiazines, for example, chlorpromazine. Patients with acute necrotizing pancreatitis are at increased risk of gastrointestinal ulceration due to local peritonitis. Their condition should be closely monitored, and if symptoms of an ulcer appear, sucralfate and acid inhibitors of gastric secretion should be used. .TABLE OF CONTENTS

3.5.6 Diet: initiation of feeding and dietary rations for long-term use

The composition of the diet for long-term feeding of sick animals depends on the medical history, in particular, on whether there was a single attack of acute pancreatitis or the patient suffers from recurrent chronic pancreatitis. In the latter case, there is no other way to prevent the occurrence of exacerbations other than transferring the animal to a special diet with low content fat It is believed that in some cases, to enhance the effect, a small amount of pancreatic enzymes should be introduced into the diet. In humans, this technique reduces pain somewhat, but it is not clear how effective it is in preventing relapses of the disease. . DipECVIM- CA, MRCVS, ILTM

Reto Neiger received his degree in veterinary medicine in 1988 in Switzerland. After this, he spent a year combining work as a veterinarian and researcher, which gave him the opportunity to obtain a degree Dr th rays, etc. Occurs without prior sensitization of the body.

Excess selenium abundantia seleni (from the Latin abundantia excess - selenum selenium) is an endemic disease caused by an excess of selenium in soils and plants. Manifested by emaciation, stunted growth, hypotension of the forestomach, softening of the horns and hooves, and hair loss.

Isosthenuria , isosthenuria (from rp. isos identical + sthenos strength + uron urine) - excretion of low-density urine, reduced concentration function of the kidneys.

Icterus- cm. Jaundice.

Ileus , ileus (from the gr. eileo I twist) - mechanical intestinal obstruction. There are I. obstructive (clogging from the inside with stones, bezoars, calculi, helminths, etc.), strangulation(rotations, strangulations, invaginations

Which is located in the abdominal cavity, near the stomach and duodenum. The gland has two main purposes - the production of digestive enzymes, which then enter the duodenum, as well as the production of a chain of hormones and insulin that enter directly into the blood.

Causes of pancreatitis in dogs

Circumstances that can lead to the onset of the disease:

• excess weight and too fatty foods;
• a sudden change in diet in a more mature pet;
• a condition that is accompanied by an increased amount of fat in the blood (hyperlipidemia, Cushing's syndrome, diabetes mellitus, idiopathic hyperlipidemia of miniature schnauzers, hyperthyroidism);
• increased amount of calcium in the blood (vitamin D intoxication, malignant tumors and hyperparathyroidism).

A direct factor in pancreatitis may be the use of certain medications, such as:

• "Novocainamide";
• loop and thiazide diuretics;
• "Metronidazole";
• "Paracetamol";
• estrogens;
• sulfonamides;
• "Ranitidine";
• "Cimetidine";
• "Azathioprine";
• "Tetracycline";
• L-asparaginase.

Other reasons:

• diseases of the bile ducts, small intestine and liver;
• damage to the pancreas;
• poisoning with organophosphorus mixtures;
• shock state (significant and prolonged decrease in blood pressure).

In most cases, the cause of a disease such as pancreatitis in a dog remains unknown.

Symptoms

Animals with pancreatitis exhibit the following symptoms:

• stooping and hunchback, as pain appears in the abdominal wall;
• bloating of the intestines (the abdomen itself);
• vomiting after eating;
• loud rumbling of the intestinal tract;
• tachycardia;
• acute pancreatitis in dogs is characterized by itchy skin, refusal to eat, lack of stool and a sudden increase in body temperature;
• the appearance of liquid, foamy and thick feces with a sour odor.

It should be noted that the initial period of the disease occurs with normal temperature and appetite in the pet.

Acute pancreatitis is primarily diagnosed by drip administration of drugs such as Sandostatin in combination with Hartmann's solution and Gordox. As a result of their use, the animal's health status quickly improves. This way you can prevent pancreatitis in dogs.

Symptoms and treatment for chronic illness in pets can be as follows:

• the animal eats as usual, but loses weight;
• the dog sheds all the time, its fur looks unhealthy;
• Therapy for persistent pancreatitis should take place while maintaining the pet’s lifelong diet.

However, such signs can also appear with other ailments. That’s why, to determine chronic pancreatitis in dogs, special diagnostics are required: ultrasound of the pancreas, blood and urine tests, as well as an x-ray.

Treatment

Therapy consists of proper diet for the animal. The necessary requirement is to fast for at least a day, then you should give your pet food in small doses. Moreover, you should feed only dietary foods with a reduced fat content. If you give food and treat your dog correctly, then it should not get sick again (provided that the nature of the disease is not chronic).

In order for the treatment of pancreatitis in dogs to be quick and effective, it is very important:

• identify the disease in time;
• stick to a strict diet;
• treat your pet with medications.

Drug therapy

Pancreatitis without complications is usually treated conservatively. To date, there are no drugs whose effects are aimed only at eliminating inflammation in the pancreas. Drugs such as Aprotinin, Dopamine (in minimal dosages) and many others have shown their effectiveness only in the laboratory. When testing these medications on animals, they showed ineffectiveness.

What means should I give?

The main goal of drug therapy is to make pancreatitis in dogs go away without complications. Symptoms and treatment must be interrelated, that is, therapy is symptomatic. How to fight the disease?

1. Performed to relieve dehydration and electrolyte disorders. For these tasks, droppers with colloidal and crystalloid liquid are used. If infusion treatment is carried out incorrectly, this can lead to the opposite result and a deterioration in the animal’s condition. The use of colloidal mixtures (plasma, solutions of polysaccharides and Dextran 70) to restore fluid volume is the main point in the treatment of the disease.
2. Analgesics. Anesthesia is needed to relieve abdominal pain. The most effective analgesic for animals is Butorphanol, which is injected intramuscularly every 8 hours.
3. Proton pump inhibitors and H2-histamine blockers. Medicines in this series (Omeprazole and Famotidine) are used to reduce the production of hydrochloric acid in the stomach.
4. Antispasmodics. Drugs of this type are used to eliminate contraction of the muscle of the main pancreatic duct. This makes it possible to reduce pressure in the pancreatic channels. To do this, a 2% solution of papaverine hydrochloride, No-shpa and a 24% solution of Eufillin are administered.
5. Corticosteroid drugs. They are used if pancreatitis in dogs is accompanied by a state of shock.
6. Antiemetic medications (Cerucal, Serenia, and Ondansetron) are prescribed for pets with uncontrollable vomiting.
7. Antibiotics. They are prescribed if there is a risk of bacterial infection. If the animal has clinical and laboratory indications of sepsis, then aminoglycosides are used, Ampicillin every 8 hours and Penicillin G every 6 hours.

In addition, with pancreatitis it is necessary to monitor blood glucose levels.

Surgery

In order to treat pancreatitis in dogs with surgery, the following indications are necessary:

• formation of pseudocysts and ulcers in the pancreas.

To determine such anomalies, in most cases an ultrasound of the abdominal cavity is performed. In addition, surgery may be performed when intensive therapy for pancreatitis is carried out, and the pet’s condition continues to become more complicated.

Acute pancreatitis is usually completely reversible and no further treatment is required.

What to feed a dog with pancreatitis?

There are special nutritional rules that must be followed when treating a disease in a pet:

1. Small portions of food.
2. Frequent feeding (the animal needs to be given food every 3-4 hours).
3. All products must be crushed to prevent spontaneous injury to the gastric mucosa.
4. The volume of carbohydrate-containing and fat-containing foods in the diet should be reduced.
5. Protein foods (fish, cottage cheese and meat) should dominate the menu.
6. It is forbidden to feed a sick pet fish and rich meat broths.
7. All acidic foods are excluded from the diet.
8. Fried food is also unacceptable.
9. Ready-made meals should be served not very hot or not very cold.
10. In case of increased pain, therapeutic fasting is prescribed (no more than 2 days).

The main rule for pancreatitis is to reduce fatty foods in the diet. This is due to the fact that fats put a considerable burden on the work of the pancreas, and during the period of its inflammation, pain begins.

It must be taken into account that even after completion of treatment, the animal may feel discomfort when eating fatty foods.

What foods can you give when you are sick?

Feeding dogs with pancreatitis can be done with special foods created specifically for them. The food contains all the necessary elements required for an unhealthy pet.

It often happens that an animal, accustomed to tasty and varied, but at the same time harmful products, does not want to eat dietary food. In such a situation, you need to be persistent and not adapt to the dog. In any case, hunger will make itself felt, and the pet will be forced to eat what is given.

In addition to feed, the animal is allowed to be given dietary meat (chicken, turkey or rabbit). It can be boiled, ground using a blender or meat grinder and mixed with rice or millet porridge. In very small doses, you can feed your dog chopped vegetables in the form of puree. It is allowed to include low-fat fermented milk products (milk and cottage cheese) in the diet.

We must not forget that small portions should be given to the pet, so as not to place an increased load on the pancreas, and also not to provoke another attack of the disease.

What products are prohibited?

Pancreatitis in dogs involves avoiding certain foods, namely:

• smoked meats, sharp cheeses, sausages;
• fresh rye bread;
• fatty fish and meat;
• beef and lamb fat;
• vegetables (corn, radish, spinach, cabbage, sorrel, greens), grains and legumes.

The body of any pet is individual; the development of pancreatitis can also be varied. In this regard, it should be borne in mind that a rational diet, its duration and composition can only be prescribed by a veterinarian. Therefore, there is no need to self-medicate.

Factors causing pancreatitis

Recently, many doctors have come to the conclusion that acute and chronic pancreatitis are a phase of one disease. Pancreatitis is a fairly common disease in small domestic animals, but the issues of diagnosis and treatment

remain complex. Diagnosis of pancreatitis is one of the most difficult both in humane gastroenterology and in veterinary medicine, which is associated with the nonspecificity of the manifestations of clinical symptoms of the disease and laboratory research methods. In veterinary medicine, diseases of the pancreas are divided into non-inflammatory (diabetes mellitus, acinar atrophy leading to exocrine pancreatic insufficiency), inflammatory (acute edematous pancreatitis, acute hemorrhagic pancreatitis, etc.), pancreatic tumors (insulinomas, adenocarcinomas) and fibrosis with pancreatic atrophy.

The factor that causes pancreatic damage in both dogs and cats often remains unknown. Provoking factors include heavy feeding of fatty foods, obesity and hyperlipidemia (in miniature schnauzers), infections (toxoplasmosis and infectious peritonitis virus in cats, parvovirus in dogs), obstruction of the pancreatic duct, ischemic and traumatic lesions of the pancreas caused by both surgery and and the injury itself, as well as a number of medications that can cause functional impairment.

Genetic predisposition. Miniature schnauzers, Yorkshire terriers, cocker spaniels, and poodles are predisposed to this disease. In German Shepherds, pancreatic acinar atrophy is hereditary and is transmitted in an autosomal recessive manner.

The pathogenesis (mechanism of development) of the disease includes autoimmune destruction of pancreatic tissue and atrophy of the acini. The affected areas of the gland decrease in size and cease to function.

Exocrine pancreatic insufficiency in dogs can develop at any age, but is more common in dogs under 4 years of age. German Shepherds and Rough Collies are predisposed to this disease. According to statistics, 70% of dogs with exocrine pancreatic insufficiency are German shepherds, and 20% are rough collies.

In cats The cause of the disease is usually pancreatitis, no genetic inheritance has been identified.

Breed predisposition

• Miniature Schnauzers, Miniature Poodles, Cocker Spaniels
• Siamese cats

Average age and age range

• Acute pancreatitis is most common in middle-aged and older dogs (over 7 years of age), with an average age of 6.5 years. The average age of acute pancreatitis in cats is 7.3 years.

Sex predisposition

• Bitches (dogs)

Risk factors (contributing to the development of pancreatitis)

• Breed
• Obesity
• Intercurrent diseases in dogs such as diabetes mellitus, hyperadrenocorticism, chronic kidney failure, neoplasia
• Recent medication use
• See also reasons

Pathophysiology

• The body has many protective mechanisms that prevent the gland from self-digesting the digestive enzymes that it secretes.
• Under certain circumstances, these natural mechanisms fail and self-digestion occurs as enzymes become activated within the acinar cells.
• Local and systemic tissues are damaged by the activity of released glandular enzymes and free radicals.

Causes
The initial causes of pancreatitis in both dogs and cats remain unknown. The following etiological factors need to be considered:

• Nutritional – hyperlipoproteinemia
• Ischemia and injury of the pancreas (pancreas)
• Duodenal reflux
• Medicines and toxins (see Contraindications)
• Pancreatic duct obstruction
• Chronic kidney disease
• Hypercalcemia
• Infectious agents (Toxoplasma and feline peritonitis virus).

Course of the disease.Pancreatitis is conventionally divided into acute and chronic. Acute pancreatitis is inflammation that develops suddenly without any prior symptoms. Chronic pancreatitis is a long-term inflammatory disease, which is often accompanied by irreversible morphological changes in the structure of the organ. Acute pancreatitis can have a mild (edematous) form or a severe form, often ending in death - in the form of hemorrhagic pancreatic necrosis. Normally, the pancreas has a number of protective mechanisms that prevent the activation of digestive enzymes in the gland itself and its self-digestion. As a result of premature activation of enzymes (trypsin, and then chymotrypsin, lipase, etc.), edema and necrosis, damage to the walls of blood vessels occur. Clinical symptoms are quite diverse. Typically, dogs experience damage to the gastrointestinal tract (vomiting, diarrhea), pain in the epigastric region, weakness, and refusal to feed. The disease very often develops some time after feeding. Severe forms of the disease are manifested by severe pain, which can quickly lead to the development of collapse and shock. This condition is characterized by a praying posture (the front legs are extended forward, the chest is on the floor, and the back of the animal is raised). In cats, symptoms are often non-specific - they can be lethargy, depression and refusal to feed.

Affected Systems

• Gastrointestinal – changes in motility (ileus) due to regional chemical peritonitis, local or generalized peritonitis due to increased permeability; hepatic damage due to shock, pancreatic enzymes, inflammatory cell infiltrates and cholestasis.
• Urinary – hypovolemia from loss of gastrointestinal secretions, which can cause prerenal azotemia.
• Respiratory—pulmonary edema, pleural effusion, or pulmonary embolism in some animals.
• Cardiovascular – Cardiac arrhythmia due to the release of myocardial depressant factor in some animals.
• Blood/lymphatic/immune – disseminated intravascular coagulation in some animals.

Clinical signs typically manifested in this disease.

Clinical signs in dogs are more due to gastrointestinal disorders.

• Clinical signs in cats are more vague, nonspecific, and nonlocalized.

• Lethargy/depression is common in cats and dogs
• Anorexia (in both species)
• Vomiting is more common in dogs due to acute inflammation, less common in cats
• Dogs may exhibit abdominal pain by showing abnormal postures.
• Diarrhea is more common in dogs than in cats

• Usually dehydration
• In some animals, fluid is felt in distended intestinal loops
• Massive damage is felt upon palpation
• Fever is more common in dogs, and fever and hypothermia have been noted in cats.
• Jaundice is more common in cats than in dogs.

Less common systemic abnormalities include respiratory distress, coagulation disorders, cardiac arrhythmias

. Let's list them point by point:

• Arrhythmia
• Heart murmur
• Muffled heart sounds
• Prolongation of capillary refill time
• Tachycardia
• Weak pulse
• Abnormal stretch
• Anorexia
• Ascites
• Bloody feces
• Reduced amount of feces
• Diarrhea
• Bloody vomiting
• Melena
• Vomiting, regurgitation
• Ataxia, incoordination
• Dysmetria, hypermetria, hypometria
• Fever, pyrexia
• Generalized weakness, paresis, paralysis
• Inability to stand
• Hypothermia
• Jaundice
• Abdominal masses
• Obesity
• Pale mucous membranes
• Petechiae and ecchymoses
• Polydipsia
• Tetraparesis
• Trembling, tremor, fasciculation
• Lack of weight, fatness
• Weight loss
• Coma, stupor
• Stupidity, depression, lethargy
• Head tilt
• Seizures and fainting, convulsions, collapse
• Anisocoria
• Nystagmus
• Colic, abdominal pain
• Pain from external pressure on the abdomen
• Abnormal pulmonary and pleural sounds
• Muffling pulmonary and pleural sounds
• Dyspnea
• Nose bleed
• Tachypnea
• Cold skin, ears, limbs
• Glucosuria
• Hematuria
• Hemoglobinuria or myoglobinuria
• Ketonuria
• Polyuria
• Proteinuria

Differential diagnosis

• Differentiate acute pancreatitis from other abdominal pain
• Perform complete blood count, biochemical, and urinalysis to rule out metabolic disease.
• Perform abdominal radiography to exclude organ perforation; generalized loss of detail indicates pleural effusion; check for organomegaly, masses, radiopaque stones, obstructive disease, and radiopaque foreign bodies.
• Perform abdominal ultrasonography to rule out the presence of masses or organomegaly.
• Perform paracentesis and fluid analysis if the patient has an effusion.
• Special studies are required, including gastrointestinal contrast radiography, excretory urography, and cytological examination.

Blood and urine tests

• Hemoconcentration, leukocytosis with a left shift, toxic neutrophils in many dogs
• In cats it is more variable and may have neutrophilia (30%) and non-regenerative anemia (26%)
• Prerenal azotemia, reflecting dehydration.
• The activity of liver enzymes (ALT and AST) is often high, as a consequence of liver ischemia and exposure to pancreatic toxins.
• Hyperbilirubinemia, more common in cats, is caused by hepatocellular injury and intra- or extrahepatic obstruction.
• Hyperglycemia in dogs and cats with necrotizing pancreatitis caused by hyperglucagonemia. Moderate hypoglycemia in some dogs. Cats with suppurative pancreatitis may be hypoglycemic.
• Hypercholesterolemia and hypertriglyceridemia are common.
• Serum amylase and lipase activities are high in some dogs, but are not a specific finding. Serum amylase and lipase activities are high in some animals with liver disease, kidney disease, or neoplasia in the absence of pancreatitis. Administration of dexamethasone may increase serum lipase concentrations in dogs. Lipase may be high or normal in cats. Amylase is usually normal or decreased in cats. In general, lipase activity is a more reliable marker in the diagnosis of pancreatitis. A normal serum lipase level does not exclude disease.
• The urine test results are normal.

Laboratory tests The diagnosis can be indirectly confirmed by an increase in the activity of pancreatic amylase and lipase in the blood, but their normal content does not exclude inflammation of the pancreas. Conversely, an increase in these indicators in the absence of clinical symptoms of the disease does not indicate pancreatitis in the animal. An increase in transaminases (ALT, AST), leukocytosis, an increase in bilirubin, and glucose are often observed. Abroad, trypsin-like immunoreactivity in blood serum is measured in animals. During ultrasound examination, even a swollen pancreas is often not visualized. An indirect sign is the presence of gas (flatulence) in the gastrointestinal tract during radiography and ultrasound of the abdominal organs.

• The trypsin immunoreactivity test (TIRT) is specific for the pancreas, and high serum concentrations are observed in some dogs and cats with pancreatitis.
• TIRT tends to increase faster and returns to normal faster than amylase and lipase levels in dogs.
• Reduced glomerular filtration may cause an increase in serum TIRT.
• Normal TIRT values ​​do not exclude pancreatitis.

ELISA for trypsinogen-activating peptide (TAP)

• Acute pancreatitis stimulates intrapancreatic activation of trypsinogen by the release of tPA into the blood serum. TPA is then excreted from the body in urine.
• The recent development of an ELISA test for tPA has made this study possible but is not yet commercially available.

This analysis is intended to be produced for specific and rapid assistance in the diagnosis of acute pancreatitis.

Diagnostics

Contrary to popular belief, amylase and lipase activity in the blood are not decisive factors for the diagnosis of pancreatitis. The fact is that, unlike in humans, in acute pancreatitis in dogs and cats the level of these enzymes can be normal, while in other diseases of the gastrointestinal tract, for example, intestinal foreign body or enteritis, their level can be high.

A sensitive test for pancreatitis recently developed at Texas A&M University, called Pancreatic Lipase Immunoreactivity (PLI), is not yet available in Ukraine.

Considering the above, to diagnose pancreatitis, the doctor must analyze the animal’s symptoms, clinical and biochemical blood test data, and the results of ultrasound and/or abdominal x-ray. Since uncomplicated pancreatitis is treated therapeutically, and its symptoms are similar to those of intestinal obstruction, the main diagnostic task that the doctor solves is to exclude pathology that requires emergency surgical intervention.

Also, to diagnose pancreatic insufficiency, the doctor uses as much data as possible about the animal, taking into account its breed, age, symptoms, data on the presence of the disease in the parents, and fecal analysis for feed digestibility.

Visual diagnostic methods
X-ray of the abdominal cavity

• Increased opacity of soft tissues in the right cranial abdominal compartment. Loss of visceral detail (ground glass) due to pleural effusion.
• The presence of static gas in the proximal duodenum.
• Widening of the angle between the pylorus and the proximal part of the duodenum.
• Delayed transit of contrast from the stomach and proximal small intestine.

X-ray of the chest cavity

• Pulmonary edema
• Pleural effusion
• Changes suggestive of pulmonary embolism

Ultrasonography

• Heterogeneous dense and cystic masses indicate pancreatic abscesses.
• Loss of normal echogenicity of the pancreas in many patients.

Other diagnostic tests

• An ultrasound-guided biopsy can confirm the diagnosis.
• Laparotomy and pancreatic biopsy may be required to identify or confirm pancreatitis.

Histopathological studies

• Edematous pancreatitis - moderate edema
• Necrotizing pancreatitis - grayish-yellow areas of pancreatic necrosis accompanied by varying degrees of hemorrhage.
• Chronic pancreatitis - the pancreas is small in size, dense, gray in color, and may contain extensive adhesions to surrounding organs.
• Microscopic changes include edema, parenchymal necrosis, and neutrophil cell infiltrate in animals with acute lesions. Chronic lesions are characterized by fibrosis of the pancreas around the ducts, hyperplasia of the ductal epithelium, and a mononuclear cell infiltrate.

Prevention

• Weight reduction for obesity
• Avoiding a high fat diet
• Avoid taking medications that can cause pancreatitis.

Possible complications

• Pulmonary edema
• Heart rhythm disturbances
• Peritonitis
• Hepatic lipidosis in cats
• Lack of response to maintenance therapy.
• Diabetes
• Exocrine pancreatic insufficiency

Expected course and forecast

• Good prognosis for animals with edematous pancreatitis. These patients usually respond well to treatment. Relapse or treatment failure occurs most often in animals that are given oral nutrition prematurely.
• Poor or guarded prognosis in animals with necrotizing pancreatitis and life-threatening complications.

Owner education (familiarization with the complexity of the disease and prognosis)

• Discuss the need for prolonged hospitalization.
• Discuss the possibility of complications such as relapse, diabetes, exocrine insufficiency.

Surgical aspects

• Surgery may be necessary to remove acute pancreatic abscess or necrotic tissue in patients with necrotizing pancreatitis.
• Extrahepatic obstruction caused by pancreatitis requires surgical correction.

Medicines and liquids.

Diet. In mild cases, a fasting diet for at least a day and painkillers and antispasmodics are indicated to reduce pancreatic secretion. In severe cases, hospitalization of the animal with intensive infusion therapy is necessary to prevent the development of such severe conditions as pulmonary edema, peritonitis, and disseminated intravascular coagulation syndrome. Analgesics (butorphanol), parenteral or enteral nutrition through a tube, plasma, and protease inhibitors (contrical) are also used in therapy. antacids and antiemetics, antisecretory drugs (Sandostatin), antioxidant drugs (Mexidol, Essentiale), antibiotic therapy, lytic mixtures, dopamine.

• Aggressive intravenous therapy is the key to successful treatment. Balanced electrolyte solutions such as Ringer's lactate are the first choice in treatment. The amount of rehydration required for the initial adjustment must be accurately calculated and administered over the first 4-6 hours.
• Colloids (dextrans and hetarstach) may be necessary to maintain pancreatic microcirculation.
• Once the deficit is corrected, additional fluids are given to support the patient's needs and ongoing losses. Potassium chloride is needed because of the normal loss of potassium through vomiting.

• Corticosteroids are only indicated for patients in shock.
• Central antiemetics for patients with intractable vomiting are chlorpromazine (every 8 hours) and prochlorperazine (every 8 hours).
• Antibiotics are necessary if the patient has clinical or laboratory evidence of sepsis - penicillin G (every 6 hours), ampicillin sodium (every 8 hours) and possibly aminoglycosides.
• Analgesics may be necessary to relieve abdominal pain: butorphanol (every 8 hours SC) is an effective treatment for dogs and cats.

Contraindications

• Avoid using anticholinergic drugs such as atropine. These drugs have variable effects on pancreatic secretions and may cause generalized suppression of GI motility, leading to ileus.
• Avoid azathioprine, chlorothiazide, estrogens, furosemide, tetracycline, and sulfamethazole.

Warning

• Use corticosteroids only in patients who are adequately hydrated due to the vasodilation effects of corticosteroids. Corticosteroids may complicate pancreatitis.
• Use phenothiazine antiemetics only in well-hydrated patients as these drugs have a hypotensive effect.
• Use dextrans cautiously in patients with hemorrhagic pancreatitis as they may promote bleeding.

conclusions

• Assessing the patient's hydration is especially important in the first 24 hours of treatment. Evaluation of results, general blood count, total plasma protein, residual urea nitrogen, body weight, diuresis - 2 times a day.
• Assess rehydration therapy after 24 hours, adjust the intensity of fluid administration and its composition accordingly. Repeat serum chemistry panel to assess electrolytes and acid-base balance.
• Repeat the plasma enzyme concentration test (eg, lipase or TIRT) after 48 hours to assess the status of the inflammatory process.
• Closely monitor for systemic complications. Perform appropriate diagnostic tests as needed (see complications).
• Gradually introduce oral nutrition as clinical signs resolve.

Likar - VOLODIMIR GENADIYOVYCH SUVOROV

ETIOPATHOGENESIS AND FEATURES:

Characteristics.
The pancreas, due to its complex anatomical location, is difficult to use with conventional physical methods of examination.
Its condition can only be judged by the dysfunction of other organs associated with it.
Insufficiency of gland function can manifest itself both in a lack of enzymes and in the inability of digestive juice to maintain an alkaline pH in the intestines.
Under these conditions, normal intestinal cavity digestion is disrupted, in thin section Microbes multiply rapidly, intestinal dysbiosis occurs, further worsening digestive processes.
Parietal enzymatic digestion (maldigestion syndrome) and absorption of enzymatic hydrolysis products (malabsorption syndrome) are disrupted.
Exhaustion increases with increased appetite (malnutrition syndrome), and the function of other endocrine glands is disrupted.

ETIOLOGY:
Exocrine pancreatic insufficiency (EPI) can be caused by pancreatic disease or pancreatic failure. Further changes are the result of a disease process that affects the regulation of pancreatic secretion and the activity of pancreatic enzymes.
Functional exocrine apancreatic insufficiency can be defined as exocrine pancreatic insufficiency not caused by morphological disease of the pancreas.
Duodenal mucosal disease (DMD). It provokes EPN through the following mechanism: the hormones cholecystokinin and secretin are synthesized in the duodenum, which cause and stimulate pancreas secretion.
The duodenal mucosa also has receptors, the irritation of which causes the release of these hormones. DMB also reduces the synthesis and release of the enzyme endocrinase, which activates trypsin by pripsinogen, and activation of trypsin plays a major role in the activation of all pancreatic proteases.

Causes of deficiency of pancreatic enzyme activity in the intestines:

1. INADEQUATE SECRETION OF THE PANCREAS:
Decreased pancreatic synthesis
Pancreas atrophy;
Congenital enzyme deficiency;
Decreased secretion of the normal pancreas
Duodenal mucosal disease
Nervous regulation disorders
Humoral regulation disorders
Slow secretion of normal pancreas. glands
Duodenal mucosal disease

2. REDUCED ENZYME ACTIVITY:
Duodenal mucosal disease
Enterokinase deficiency
Lack of bile acids
Decreased lipase activity
Reduced trypisinogen activity due to enterokinase.

3. INTESTINAL FACTORS DECREASING ENZYME ACTIVITY:
Extremely acidic optimum pH activity
Low gastric emptying rate
Duodenal mucosal disease
Affected by enterogastron-mediated reflex
Affected by the enterogastric reflex
Overfeeding
Decreased level of pancreatic secretion
Deficiency of bicarbonate secretion
Reduced level of proteolytic breakdown of enzymes
Bacterial proteases
Hyperreproduction of microflora caused by:
Stasis
Obstruction
Hypomobility

PATHOGENESIS:
the mucous membrane of the small intestines (especially the duodenum) synthesizes the hormones cholecystokinin and secretin, which stimulate pancreatic secretion. There are receptors in the mucosa that help the release of these hormones. The duodenal mucosa has a very high concentration of receptors and endocrine secretory cells, but pancreatic secretion can also be simulated by jejunal hormones. Any chronic mucosal disease therefore inhibits the secretion of pancreatic products.
Their increased degradation by digestive enzymes has a similar effect. This occurs when proteases that are destroyed are in deficiency due to mucosal atrophy or other pathology, which makes them active and they inactivate pancreatic enzymes that are secreted in sufficient quantities.

FEATURES: chronic pancreatitis and juvenile pancreas atrophy -
- the most common causes of exocrine pancreatic insufficiency.

Summary clinic:
1. Anorexia (lack of appetite, refusal to eat);
2. Tousled fur;
3. Diarrhea;
4. Exhaustion, cachexia, unkemptness;
5. Unusual or foul-smelling stool;
6. Polydipsia, increased thirst;
7. Polyphagia, extremely increased appetite;
8. Loss of body weight;
9. Vomiting, regurgitation, emesis;
10. Steatorrhea, fat in stool;
11. Enlarged borborygms, flatulence;
12. Depression (depression, lethargy);
13. Flatulence;

Symptoms Endocrine pancreatic insufficiency is characterized by: polydipsia and polyuria, vomiting, flatulence (discharge of foul-smelling gases), pancreatogenic diarrhea (smelly, with frequent bowel movements and an increase in the volume of feces, not amenable to therapy), pancreatogenic stool (polyfecal - bulky stool in the form of foamy, soft, spongy colorless masses with a sour odor, a greasy sheen and undigested food debris, sometimes mixed with blood), polyphagia up to coprophagia, flatulence in all parts of the intestine, hyperglycemia, glucosuria, hypocholesterolemia, increased amylase levels in the blood serum, steatorrhea, creatorrhoea, amilorrhea, acidity feces.

Diagnosis: based on:
- clinical signs;
- examination of feces for the presence of traces of muscle fibers;
- examination of feces for the presence of fats;
- tests for the level of protein processing;
- BT-PABA tests;
- 72-hour fecal tests for fats or serum trypsin-like immunoreactivities measured by radioimmunoassays;
- influence of exposure to pancreatic enzymes;

It is not always possible to make a diagnosis while the animal is alive.
If the listed symptoms are detected during examination, there is reason to suspect pancreaopathy.
Ascites in combination with hyperglycemia also indicates the participation of the pancreas in the pathological process.
To be more confident in making a diagnosis, one or two functional tests are performed.

Differential diagnosis.
Symptoms of exocrine pancreatic insufficiency must be distinguished from polyphagia caused by chronic enteritis and various types of malabsorption.
Pancreaopathy is characterized by polyphagia against a background of progressive cachexia. The activity and performance of the animal can be maintained for a long time, which is not typical for chronic enteritis and hepatopathy (rapid increase in depression, temporary or long-term loss of appetite).
Pancreaopathy is also distinguished by concomitant bradycardia; in contrast to enterocolitis, defecation is frequent, but there is no tenesmus.

TREATMENT, DEVELOPMENT AND PROGNOSIS:

MEDICATION:
- Mezim forte: 1-2 tblt/day for 5-7 days;
- Trizim: 1-2 tblt/day for 5-7 days;
- Cimetidine: 5-10 mg/kg/8 hours/per os;
- Neomycin (Neomicin) sulfas: 2.5-10 mg/kg/per os/6-12 hours;

Additional - symptomatic:
- Spasmolyt: initially once 1 ml/10 kg/iv;

DEVELOPMENT: acute, with a tendency to become chronic.

FORECAST: doubtful to favorable.